Nutritional attributes of tomatoes

Full text

Crop & Food Research Confidential Report No. 1391
Nutritional attributes of tomatoes
L J Hedges & C E Lister
June 2005
A report prepared for
VegFed
Copy 9 of 9
New Zealand Institute for Crop & Food Research Limited
Private Bag 4704, Christchurch, New Zealand

Contents
1 Executive summary 1
1.1.1 Background 1
1.2 Composition 1
1.3 Lyopene and human health 1
1.4 The role of other tomato components in human health 1
1.5 Bioavailability 2
1.6 Tomato consumption and major disease patterns 2
1.7 Optimum intake levels 2
1.8 Factors affecting phytochemical levels in tomatoes 2
1.9 Promoting nutritional benefits 2
2 Introduction 3
3 Composition 4
3.1 Antioxidant vitamins 6
3.2 Carotenoids 6
3.3 Phenolic compounds 13
4 Lycopene and human health 17
4.1 Proposed mechanisms of action 17
4.2 Prostate cancer 18
4.2.1 Epidemiologic studies 18
4.2.2 Prospective studies 19
4.2.3 Case-control studies 19
4.2.4 Clinical studies/blood and tissue studies 20
4.3 Lycopene and other cancers 21
4.3.1 Skin cancer 21
4.3.2 Cancers of the digestive tract 22
4.3.3 Breast cancer 23
4.3.4 Ovarian and cervical cancer 23
4.3.5 Bladder cancer 24
4.3.6 Lung cancer 24
4.4 Cardiovascular disease 24
4.5 AIDS 26
4.6 Diabetes 26
4.7 Eye disease 26
H:\rpt2005\1391.doc

5 The role of other tomato components in human health 27
5.1 Other carotenoids 27
5.2 Phenolic compounds 28
5.3 Other 28
6 Bioavailability of tomato phytochemicals 29
6.1 Lycopene 29
6.2 Other carotenoids 32
6.3 Phenolics 34
7 Tomato/lycopene consumption and major disease
patterns 36
8 Factors affecting phytochemical levels in tomatoes and
tomato products 38
8.1 Lycopene and other carotenoids 38
8.1.1 Cultivar 38
8.1.2 Growing conditions 40
8.1.3 Degree of ripeness and postharvest storage 41
8.1.4 Effects of cooking/processing 42
8.2 Phenolics 46
8.2.1 Raw tomatoes 46
8.2.2 Processing/cooking 47
8.3 Vitamins 48
8.4 Summary 49
9 Promoting nutritional attributes 49
10 References 50
Appendices 69
Appendix I 69
Appendix II 70
H:\rpt2005\1391.doc

Nutritional attributes of tomatoes
L J Hedges & C E Lister, June 2005
Crop & Food Research Confidential Report No. 1391
New Zealand Institute for Crop & Food Research Limited
Page 1
1 Executive summary
1.1 Background
This report is intended to provide an information resource from which material
can be selected for incorporation into promotional and educational booklets
for the various VegFed sector groups. We have gathered relevant literature,
including medical research and scientific papers, and, where possible,
information specific to New Zealand. This report focuses on the nutritional
attributes of tomatoes, but also includes factors that may influence these,
such as bioavailability, agronomical issues, cooking or processing and
storage. Some additional material of general interest has also been included.
1.2 Composition
Tomatoes contain a variety of phytochemicals, the most well known being
lycopene. In addition, other carotenoids (e.g. β-carotene, phytoene,
phytofluene), phenolics (e.g. coumaric and chlorogenic acids, quercetin, rutin
and naringenin), moderate amounts of the antioxidant vitamin C (ascorbic
acid) and a little vitamin E (tocopherol) are present. Carotenoids are present
in many vegetables and fruit but lycopene is more restricted in its distribution,
being concentrated in tomatoes, guava, rosehip, watermelon and pink
grapefruit. Lycopene imparts the red colour to these fruits.
1.3 Lyopene and human health
Globally, considerable research is being conducted into the health benefits of
lycopene. It is a powerful antioxidant; antioxidants neutralise free radicals,
which may cause damage to cell components (e.g. DNA, protein, lipids). It
may also have a range of other modes of action. The strongest scientific
evidence is for a role of lycopene in reducing the incidence of prostate
cancer. Lycopene may also help reduce the incidence of other cancers and
cardiovascular diseases, and play a role in eye health.
1.4 The role of other tomato components in human
health
There has been less study of the role of other tomato phytochemicals. β-
Carotene is an important precursor of vitamin A and, like lycopene, may play
a role in cancer prevention. The phenolic compounds, especially the
flavonoids, are important antioxidants. Other potential health-promoting
bioactivities of the flavonoids include anti-allergic, anti-inflammatory, anti-
microbial and anti-cancer properties. The yellow jelly around tomato seeds
may stop platelet aggregation and help prevent heart attacks, strokes and
blood vessel problems.

1.5 Bioavailability
Lycopene is absorbed in the human body and is one of the most common
circulating carotenoids. Other tomato carotenoids may also be bioavailable.
Many factors affect the bioavailability of lycopene and other carotenoids,
including the nature of the food matrix, thermal processing and presence of
fat. Of the phenolics, naringenin from tomatoes has been shown to be
bioavailable. Data on other phenolics are lacking.
1.6 Tomato consumption and major disease patterns
New Zealanders would appear to consume fewer tomato and tomato-based
products than do Mediterranean peoples and have a higher incidence of
prostate cancer. Heart disease mortality figures are also higher. Whether
these higher incidences of disease are related to lower tomato consumption
remains to be proven, but this association may at least be part of the answer.
1.7 Optimum intake levels
To date there is no clear consensus on the intake of lycopene required to
reduce disease risk. Suggestions range from about 5 up to 35 mg lycopene
per day. This could be achieved by consuming at least one or two servings of
tomatoes or tomato products every day.
1.8 Factors affecting phytochemical levels in tomatoes
Levels of tomato phytochemicals may be affected by cultivar, growing
conditions, degree of ripeness and cooking or processing. It may be possible
to enhance the levels of lycopene and other phytochemicals in tomatoes and
tomato products by managing these factors.
1.9 Promoting nutritional benefits
Since lycopene intake levels are comparatively low in New Zealand
compared to in Mediterranean countries, promotion could build on the notion
that tomato consumption may reduce disease incidence, particularly that of
some cancers and cardiovascular disease. Prostate and skin cancer could be
of special interest because of their high levels of occurrence here.
The intense red colour and therefore high lycopene content of some New
Zealand-grown tomatoes over the paler Australian imports could be a
differentiating factor for promotional purposes.
Consumption of the whole tomato, including skins and seeds, consumed with
a little good quality oil optimises the delivery of the potential benefits of
tomatoes in general, as well as lycopene specifically. Cooking also enhances
lycopene bioavailability, but can also reduce levels of other nutrients, such as
vitamin C.
Page 2

2 Introduction
The much heralded ‘Mediterranean diet’ is widely believed to confer health
benefits with respect to preventing particular cancers and cardiovascular
disease. It typically contains a significant proportion of fruit and vegetables,
cereals, fish, olive oil and red wine. Initially, the general components of this
diet were studied and the benefits of the Mediterranean diet attributed
variously to the high amounts of fibre, the high vitamin intake, and the omega
3 polyunsaturated fish oils and omega 6 polyunsaturated oils in whole grains
and monounsaturated olive oil. More recently, the contributions made by
antioxidants and other phytochemicals, such as the sulfur compounds
present in the onion family and the phenolics in red wine, have been
recognised. More recently still, attention has turned to the ubiquitous tomato
and the pigment that gives it the characteristic red colour, lycopene.
Originating from South America, and taken back to Europe by the Spaniards
in the early 16th century, the tomato was initially viewed with suspicion in
northern Europe and English speaking countries where it was also known as
the “wolf peach”. A rough translation of its botanical name, Lycopersicon, is
“edible wolf peach”, which is an echo of this. Nowadays, however, it is widely
cultivated and consumed worldwide, although particularly prominent in Italian,
Spanish, Greek and Mexican cuisine. It is frequently consumed fresh as a
salad vegetable, but is also processed into a wide range of products including
ketchup, soup, puree, paste, pasta sauces; canned in various forms; and
combined with various other vegetables, herbs and spices. Salsa is an
increasingly popular product. It has been estimated that in the United States
more salsa is now consumed than ketchup (Virginia Tech 2003). In the
United States and Australia it is the second most commercially important
vegetable crop after potatoes (Yeung & Rao 2001; Australian Bureau of
Statistics 2003). In New Zealand, consumption of fresh and processed
tomatoes is second only to potatoes (VegFed 2005).
There is a large array of commercially available cultivars, reflecting the
plant’s adaptability for different growing conditions and end uses. The fruit
produced ranges from as small as 1.5 cm in diameter and weighing about 8 g
to around 18 cm in diameter and weighing about 800 g (Yeung & Rao 2001 -
units converted to metric). They can vary also in colour from white to red to
purplish black, including green, yellow and orange, as well as in shape
(Yeung & Rao 2001). In red tomatoes some researchers maintain that it is
often only the flesh that supplies the red colour, the skin itself often being
yellow or orange (Virginia Tech 2003). However, other reports state that the
skins contain more lycopene, the red pigment, than the pulp (Sharma & Le
Maguer 1996). A New Zealand study of three hydroponically grown
greenhouse cultivars. similarly found that on a per weight basis the skins
contained more lycopene than the pulp, but that when considering the fruit as
a whole, more lycopene was provided by the pulp (Toor & Savage 2005).
This report provides information on the nutritional attributes of tomatoes and
their role in a healthy diet. It also describes factors that may affect these
attributes. Additional material of general interest is provided in Appendix I.
Page 3

3 Composition
The major nutritional components of the tomato are shown in Table 1. Further
data on the nutritional composition of fresh tomatoes and tomato-based
products are given in Appendix II. As can be seen, tomatoes are a good
source of vitamin C and vitamin A equivalents (in the form of β-carotene, see
Section 3.2) and also provide some vitamin E, folic acid, potassium and other
trace elements. Protein and dietary fibre are also present, although the major
constituent is water, comprising 94-95% of the fruit by weight (Davies &
Hobson 1981). Processed tomatoes may have higher levels of some
nutrients because their concentration may be higher in these forms.
Vitamin C is important to prevent scurvy but it is also a powerful antioxidant
and may help prevent a range of degenerative diseases. It has been
estimated that tomato production in the United States could provide about
one-third of the recommended dietary allowance (RDA) for Americans
(Pantos & Markakis 1973). The actual contribution to the vitamin C supply is
considerably lower than this (12.2% in 1972), but nevertheless only oranges
and potatoes contribute more to the American diet (Senti & Rizek 1975).
Another nutritionally important component is β-carotene, since it is converted
to vitamin A in our bodies. Vitamin A is important for night vision,
maintenance of skin, immune function and prevention of infections.
Potassium is an essential nutrient for normal health maintenance and growth.
Potassium, along with calcium and magnesium, may play a role in reducing
high blood pressure. Dietary fibre is important to maintain a healthy digestive
system and may also help to control high cholesterol levels in the blood.
Tomatoes are a considerable source of fibre, especially when eaten with the
skin and seeds.
Table 1: Major dietary components per 100 g red raw tomato.
1 NZ Food Composition Database (Athar et al. 2001).
2 USDA National Nutrient Database for standard reference, Release 15 - Year round
average.
3 Data from Yeung & Rao (2001).
Nutrient NZ1USA2Other3
Vitamin A 92 µg RAE 31 µg RAE; 623 IU 1000 IU
Vitamin B1 (µg) 20 59 60
Vitamin B2 (µg) 10 48 40
Folic Acid (µg) 14 15 28
Vitamin C (mg) 23.7 19.1 22
Vitamin E (mg) 0.77 0.38 1.2
Potassium (mg) 265 222 290
Calcium (mg) 11 5 21
Magnesium (mg) 12.1 11 14
Page 4

In addition to the general nutrients above, tomatoes contain an array of
phytochemicals (= plant-derived chemicals). Many of these compounds are
antioxidants, substances that inactivate certain harmful reactive compounds
in the body (free radicals). There are many different antioxidants, including
vitamins C (ascorbic acid) and E (tocopherols), carotenoids, flavonoids and
other phenolics, the trace elements selenium and zinc, some sulfur
compounds and other individual substances (e.g. lipoic acid and coenzyme
Q). These antioxidants are substances that have beneficial effects in the
body beyond providing the nutrients necessary to prevent deficiency
diseases such as scurvy, pellagra and beriberi. Instead, they are believed to
prevent or delay the onset or progression of many chronic diseases, such as
cancer and cardiovascular disease. They may deactivate free radicals that
may be present in the body through diet, pollution, smoking, exposure to
radiation or UV light or merely as part of the body’s normal processes. As can
be seen from Table 2, tomatoes contain a significant number of these
antioxidants and in reasonable quantities. Of these, lycopene is of particular
interest since it is available in relatively few other foods, yet is present in
tomatoes in reasonable quantities.
The levels of these antioxidant components may vary according to such
factors as cultivar (Hayman 1999; Orlowski et al. 2002; Thompson et al.
2000), growing conditions (Lacatus et al. 1995; Zushi & Matsuzoe 1998),
method of ripening (Arias et al. 2000), processing (Shi & Le Maguer 2000;
Thompson et al. 2000; Takeoka et al. 2001) and storage conditions (Hayman
1999). These agronomic issues will be discussed in greater detail in Section
8. As will be seen, some of these micronutrients are destroyed by processing
but with others, such as lycopene, bioavailability may be enhanced.
Table 2: Summary of the levels of the main antioxidant components in
tomatoes (data from a range of sources).
Component
Typical concentration
(mg/100 g FW)
Ascorbic acid 15-48
Carotenoids (total) 4-24
β-carotene 0.4-1
lycopene 3-18
phytoene 1-3
phytofluene ~1
Phenolic acids 16-29
caffeic acid 0.2-10
chlorogenic acid 1.3-3.8
coumaric acid 0.1-1.6
ferulic acid 0.1-0.7
Flavonoids
naringenin 0.4-4.2
quercetin glycosides (primarily rutin) 0.3-4.3
kaempferol glycosides 0.02-0.10
Vitamin E 0.04-1.2
Page 5

3.1 Antioxidant vitamins
Tomatoes contain high levels of vitamin C (Fig. 1) and it has been stated that
for Americans tomatoes and tomato products are the third most important
source of this, after citrus fruit and potatoes (Senti & Rizek 1975). Besides
preventing scurvy, vitamin C is a powerful antioxidant, scavenging practically
all free radicals and oxidants, protecting membranes from oxidative damage
and working in combination with vitamin E to inhibit low density lipoprotein
(LDL) oxidation. It also assists the proper functioning of certain enzymes.
Only a minor amount of vitamin E (Fig. 1) is present in tomatoes, mostly in
the seeds. Besides its function as a vitamin, there is increasing evidence of
its role as an antioxidant, particularly with respect to protecting against
cardiovascular disease. There is evidence that vitamin E has synergistic
effects in combination with certain other antioxidants.
OC
COH
COH
CH
OH H
O
CH2OH
CH3
CH3
OH
CH3
O
vitamin C
(ascorbic acid)
vitamin E (alpha-tocopherol)
Figure 1: Chemical structures of vitamins C (ascorbic acid) and E (tocopherol).
3.2 Carotenoids
Yellow, orange, and red carotenoids are among the most widespread and
important natural pigments. They are found in higher plants, algae, fungi and
bacteria, both in nonphotosynthetic tissues and in photosynthetic tissue,
(where they accompany the chlorophylls). Their name is derived from the
main representative of their group, β-carotene, the orange pigment first
isolated from carrots. The carotenoids are classed into two main groups: (1)
carotenes that are hydrocarbons (C40H56), and (2) their oxygenated
derivatives (xanthophylls). Carotenoids are lipids and can specifically absorb
light in the UV and specific visible regions of the spectrum, the rest of the
spectrum is transmitted or reflected and they appear coloured. The particular
structure of individual carotenoid compounds influences their colour.
The main carotenoids present in tomatoes are shown in Tables 2 and 3, and
the structures of some of these compounds are shown in Figure 2. The red
colour of the tomato is due to its major carotene, lycopene, which is present
at levels up to 90% of the total carotenoids. A range of other carotenoids is
commonly reported including β-carotene, δ-carotene, γ-carotene and
neurosporene (Gross 1991), but reports sometimes include other
Page 6

carotenoids. Lycopene epoxide, an oxidation product of lycopene, was
reported as the second most predominant carotenoid in tomatoes (Khachik et
al. 1992). Abushita et al. (2000) also report that it was present, but at lower
levels. The common red tomato also contains the colourless precursors
phytoene and phytofluene. Composition of carotenoids does vary
considerably between cultivars. Some tomato strains are orange because
they do not synthesise lycopene or because other carotenes, such as β-
carotene, predominate. The composition of tomato seeds is slightly different
than the flesh, with lutein being the main carotenoid followed by β-carotene
and lycopene (Rymal & Nakayama 1974).
Table 3: Carotenoid content (mg/100 g FW) of tomatoes and selected tomato products
(fresh data from Dumas et al. (2003) and processed data from Tonucci et al. (1995), as
given in Beecher (1998)).
Tomato product
Carotenoid
Vitamin A
activityaFresh
tomatoes
Canned
tomatoes
Tomato
catsup
Tomato
sauce
Phytoene - 1.8 1.9 3.4 3.0
Phytofluene - 1.1 0.8 1.5 1.3
zeta-Carotene - 0.1 0.2 0.3 0.8
Neurosporene - tb1.1 2.6 7.0
Lycopene - 4.1 9.3 17.2 18.0
gamma-Carotene + tb1.5 3.0 3.2
beta-Carotene ++ 0.8 0.2 0.6 0.5
a Vitamin A activity based on similarity of chemical structure or part of carotenoid molecule to retinal.
b Trace.
Lycopene comprises a long straight chain, with 11 conjugated double bonds
(double bonds on adjacent carbon atoms) (Fig. 2). This structure is not only
responsible for conferring colour, but also for its physical properties, chemical
reactivity and its biological activity. It exists as various isomers (Fig. 3), but in
fresh fruit is usually in the all-trans configuration. However, during the heat
treatment involved in cooking or processing, exposure to light and some
chemical reactions, some lycopene may be converted to the cis
configuration. This change in the geometry of the molecule is significant
because it appears to make lycopene more bioavailable. This is discussed
further in Sections 6 and 8.1.4.
Page 7

OH
OH
lycopene
beta-catotene
phytoene
phytofluene
lutein
Figure 2: Chemical structures of lycopene and the other main carotenoids present in tomatoes.
Page 8

15-cis-lycopene
13-cis-lycopene
5-cis-lycopene
6-cis-lycopene
Figure 3: The chemical structure of cis-isomers of lycopene.
Page 9

Lycopene is only present in a few foods, the most common being tomatoes,
with watermelon, pink grapefruit, guava, red papaya and rosehips being other
sources. Tomatoes, however, are abundant, cheap, versatile and
commercially useful, making them by far the most predominant dietary
source (Bramley 2000). Table 4 below gives the lycopene content of various
foods. The lycopene content of fresh tomatoes can vary from virtually none
up to 18 mg/100 g FW, but most values for typical red tomatoes are between
5 and 8 mg/100 g FW (Dumas et al. 2003). Some reports state that lycopene
is not present in significant quantities in the tomato skin. However, Sharma &
Le Maguer (1996) state that skins contain about five times more lycopene
than the pulp (54 mg/100 g FW compared to 11 mg/100 g FW). Toor &
Savage (2005) found lycopene in the skin of the three varieties tested
averaged around three times more than in the pulp, with a small amount also
present in the seeds (although in this study the jelly around the seeds was
considered to be ‘seed’ rather than ‘pulp’).
Table 4: Lycopene content (mg/100 g FW) of fruit
and tomato products (data from Bramley (2000),
Holden et al. (1999), Rao & Agarwal (1999), Hart
& Scott (1995), Tonucci et al. (1995) and Yeung &
Rao (2001).
Food
Lycopene content
(mg/100 g FW)
Watermelon 2.3-7.2
Pink guava 5.4
Pink grapefruit 0.5-4.0
Papaya 2.0-5.3
Fresh tomato (raw) 0.9-18.1
Canned tomatoes 4.5-9.7
Tomato sauce 6.2-14.1
Tomato paste 5.4-42.2
Tomato puree 16.7
Tomato juice 5.0-11.6
Tomato ketchup 9.9-17.0
Tomato soup 5.0-7.2
Pizza sauce 12.7
As with many constituent nutrients in plants, levels of lycopene may vary
according to cultivar, maturity, growing conditions, harvesting, storage and
processing (for more discussion of this see Section 8.1). The levels of
lycopene in processed tomato products are significantly higher than in the
fresh product. It appears that processing may in fact enhance lycopene
content, firstly due to a concentration factor but also by making it more
bioavailable (Stahl & Sies 1992). Two major reasons have been postulated
for this. Firstly, the act of processing breaks down the food matrix, releasing
Page 10

Page 11
lycopene for absorption. It is also believed that the cis-isomer formed after
the thermal energy of cooking or processing is more absorbable than the all-
trans isomer (Boileau et al. 1999). For further discussion of bioavailability see
Section 6.
In addition to lycopene, a range of other carotenoids is present in tomatoes.
The most significant of these is probably β-carotene, which attracts
considerable interest nutritionally as it can be converted to vitamin A in the
human body while lycopene cannot. As mentioned earlier, cultivar has a big
influence on the presence/absence of other carotenoids. However, the
composition of carotenoids appears to be reasonably consistent over a range
of tomato products (Table 5).

Page 12
Table 5: Carotenoid content (mg/100 g FW) in tomatoes and various tomato products (from Tonucci et al. 1995).
Carotenoid
Sample β-Carotene γ-Carotene δ-Carotene Lutein Lycopene Neurosporene Phytoene Phytofluene
Lycopene-
5,6-diol
Whole tomatoes 0.23 1.50 0.21 0.08 9.27 1.11 1.86 0.82 0.11
Catsup
0.59 3.03 0.33 nda17.23 2.63 3.39 1.54 0.18
Spaghetti sauce 0.44 3.02 0.34 0.16 15.99 3.15 2.77 1.56 0.17
Tomato paste 1.27 9.98 0.84 0.34 55.45 6.95 8.36 3.63 0.44
Tomato puree 0.41 2.94 0.25 0.09 16.67 2.11 2.40 1.08 0.17
Tomato sauce 0.45 3.17 0.29 t b 17.98 2.48 2.95 1.27 0.16
a Not detected.
b Trace.

3.3 Phenolic compounds
Other phytochemicals present in tomatoes, though less studied than the
carotenoids, are the phenolic compounds. Phenolic compounds are a large
group of secondary plant products, present in most if not all plants, that differ
in chemical structure and reactivity. The chemical structures range from quite
simple compounds like caffeic acid to highly polymerised substances like
tannins. Their contribution to the pigmentation of plants is well recognised
(the anthocyanins may be red, blue or purple). However, not all phenolics are
coloured. There are numerous different groups of phenolics but the most
common phenolics found in foods are generally phenolic acids, flavonoids,
lignans, stilbenes, coumarins and tannins (Harbourne 1993). The first two of
these groups are present in significant amounts in tomatoes.
Various total phenolic levels for fresh tomatoes have been reported in the
literature: 15.82-22.68 mg/100 g FW (Davies & Hobson 1981), 23 mg/100 g
FW (Brune et al. 1991), 25.9-49.8 mg/100 g FW (Martinez-Valverde et al.
2002), and 13.15 mg/100 g FW (Minoggio et al. 2003). There are a number of
different groups of phenolic acids present, with the main ones being phenolic
acids and flavonols (rutin) (Table 2). The structures of the main phenolics
present in tomato fruit are shown in Figure 4. No data were found on the
phenolic composition of tomato seeds.
OH
OH
OH
O
rutin
O
OH OH
OH
OH
H
O
OH
OH
O
O
OH
O
OH
OH
OH
OH
CO2H
Quercetin-3-rutinoside Naringenin
Coumaric acid Chlorogenic acid
Figure 4: Chemical structures of the main phenolics in tomato fruit.
Page 13

A range of phenolic acids is present, the main ones being caffeic and
chlorogenic acids (Table 2). Some authors report that coumaric acid is the
main phenolic acid (e.g. Machiex et al. 1990) while others report chlorogenic
acid (e.g. Minoggio et al. 2003). These differences could be due to
variety/cultivar. Other phenolic acids such as coumaric, ferulic, sinapic,
vanillic and salicylic acids may also be present in smaller amounts (Davies &
Hobson 1981; Machiex et al. 1990). Cultivars vary in phenolic acid levels and
composition (Table 6). There are limited data on the distribution of phenolic
acids in the fruit, with most indicating similar contents in flesh and skin. The
total hydroxycinnamic acid level of the skin has been reported as 9.4 mg/100
g, while the flesh contains 8.4 mg/100 g (Macheix et al. 1990). However,
Herrmann (1973) reported that chlorogenic acid was as high as 50 mg/100 g
FW in tomato skin.
Table 6: Content of hydroxycinnamic acids (mg/100 g FW) in tomato
cultivars (adapted from Martinez-Valverde et al. 2002).
Phenolic acid
Tomato
cultivar Chlorogenic Caffeic p-Coumaric Ferulic
Rambo 2.79 0.26 0.11 0.19
Senior 3.28 0.14 0.13 0.17
Ramillete 2.61 1.30 0.40 0.38
Liso 3.28 0.14 nda0.16
Pera 1.43 1.23 0.25 0.32
Canario 1.70 1.29 0.24 0.27
Durina 2.23 0.99 0.42 0.54
Daniella 1.47 0.59 0.58 0.30
Remate 2.32 0.24 nda0.19
a Not detected.
Tomatoes also contain flavonols, which belong to a sub group of the
phenolics family and have been shown to have potent antioxidative activity
(Shahidid & Wanasundara 1992). Quercetin glycosides have very high
antioxidant activity relative to α-tocopherol (vitamin E) (Hertog et al. 1992).
Total flavonol levels for whole tomatoes have been reported to vary between
0.13 and 4.4 mg/100 g FW (Davies & Hobson 1981; Stewart et al. 2000;
Martinez-Valverde et al. 2002). However, typical red tomatoes usually contain
around 0.5–2 mg/100 g FW of flavonols (Table 7).
Page 14

Table 7: Content of flavonoids (mg/100 g FW) in tomato cultivars
(adapted from Martinez-Valverde et al. 2002).
Flavonoid
Tomato cultivar Quercetin Kaempferol Naringenin
Rambo 0.72 nda0.69
Senior 1.72 nda0.49
Ramillete 2.87 0.21 0.81
Liso 1.25 nda0.51
Pera 1.03 0.12 nda
Canario 2.81 nda0.85
Durina 2.23 nda0.95
Daniella 4.36 nda1.26
Remate 2.13 nda0.45
a Not detected.
The main flavonol in tomatoes is a quercetin glycoside, rutin (quercetin 3-
rutinoside), but other quercetin and kaempferol glycosides may be present in
some cultivars in small amounts (Macheix et al. 1990). As with many
phytochemicals, the flavonol content may vary according to many factors
including cultivar, the size of the fruit, maturity and environmental/growing
conditions (factors influencing the phenolic levels in plants have been
reviewed by Parr & Bolwell (2000)) Stewart et al. (2000) showed that the
highest concentration of flavonols occurs in tomato skins (Table 8), and thus,
in general, smaller tomatoes have higher amounts of this on a per weight
basis because of their higher surface area to weight ratio. Purple fruit, which
contain anthocyanins, contain much higher levels of flavonols than standard
cultivars (Table 9). The rutin level apparently drops during ripening (Macheix
et al. 1990). Levels of quercetin glycosides dropped from 1.2-2.4 mg/100 g
FW in immature green fruit to 0.3-0.7 mg/100 g FW in red fruit (Davies &
Hobson 1981). Woldecke & Herrmann (1974) also reported that the flavonol
content, on a per weight basis, decreased during the development of tomato
fruits; and it was higher in field-grown than in glasshouse tomatoes. See
Section 8.2 for further discussion of factors affecting phenolics in tomatoes,
including processing.
Page 15

Table 8: Distribution of flavonols (mg/100 g FW) in Spanish cherry
tomatoes (adapted from Stewart et al. 2000).
Tomato
Free
quercetin
Free
kaempferol
Conjugated
quercetin
Conjugated
kaempferol
Total
flavonol
Whole 0.02 0.05 2.34 0.12 2.53
Skin 0.07 0.04 13.78 0.44 14.33
Flesh nda0.01 0.09 0.02 0.12
Seed 0.01 0.02 0.1 0.02 0.15
a Not detected.
Table 9: Flavonol content (mg/100 g FW) of skins of different coloured tomatoes (adapted from Stewart
et al. 2000).
Tomato cultivar Skin colour Free
quercetin
Free
kaempferol
Conjugated
quercetin
Conjugated
kaempferol
Total
flavonol
Noire
Charbonneuse
Red/purple 0.39 0.02 40.2 1.42 44.0
Anthocyanin
Gainer
Deep red 0.30 0.04 25.2 2.09 27.6
Aubergine Red/dark
patches
0.03 nda10.3 0.45 10.8
Anthocyanin Free Red 0.06 0.01 20.6 1.73 22.4
Dark Green Red/yellow 0.08 nda18.3 0.49 18.9
a Not detected.
Another group of flavonoids present in tomatoes are the flavonones, with the
main one being naringenin (Macheix et al. 1990). Some reports state that
naringenin is present in the free form only (Wardale 1973), but others clearly
show a naringenin glycoside is also present (Hunt & Baker 1980). Hunt &
Baker (1980) reported the presence of chalconaringenin (also called
naringenin chalcone), naringenin and naringenin-7-glucoside. As with the
flavonols, levels of naringenin vary between cultivars (Table 7). Flavan-3-ols
are not present and nor are anthocyanins, except in a few unusual lines
(Macheix et al. 1990).
It has been postulated that phenolic compounds could be responsible for the
antioxidative activity in tomatoes beyond that accounted for by their lycopene
content (Takeoka et al. 2001). Other studies, including our own, have found
that in many assays the phenolics actually make a greater contribution to
antioxidant activity than the carotenoids.
Page 16

4 Lycopene and human health
Most research on lycopene has been undertaken by researchers working on
prostate cancer and cardiovascular disease. As knowledge about this
compound has increased, however, so too has interest in its possible effect in
a number of health areas, including other cancers (skin, breast, bladder,
cervix, lung, digestive tract, and female reproductive organs), osteoporosis,
and diabetes. Although it is still too early to draw conclusions, results are
promising in many of these areas. In addition, research is continuing to
expand our understanding of the metabolism of lycopene and its mode of
action.
4.1 Proposed mechanisms of action
Lycopene first caught the interest of the scientific community in the late
1980s when it was found that of all the carotenoids, including the better
known β-carotene, it was the most potent quencher of the highly reactive
compound, singlet oxygen (Di Mascio et al. 1989). It is also a potent
scavenger of peroxyl radicals (Mortensen & Skibstead 1997; Woodall et al.
1997) and nitrogen dioxide (Bohm et al. 1995). By increasing lycopene levels
in the body, oxidative stress is reduced and antioxidant potential increased.
Antioxidative activities are believed to reduce damage to lipids, both
lipoproteins and membrane lipids (Tsuchiya et al. 1993), proteins, particularly
enzymes, and DNA (Clinton 1998). There is a range of other possible modes
of action for lycopene (Fig. 5). Lycopene may regulate gene functions (Siler
et al. 2004), improve intercell gap junction communication (Zhang et al.
1997), moderate hormone function and immune response or regulate
metabolic pathways (Rao & Argawal 2000). It is also possible that these
mechanisms are interrelated and operate simultaneously. There may also be
other modes of action that have not yet been uncovered.
Page 17

Figure 5: Proposed mechanisms for the role of lycopene in preventing chronic diseases
(from Rao & Argawal 2000).
4.2 Prostate cancer
4.2.1 Epidemiologic studies
Epidemiologic studies (also called observational or population studies) look at
disease patterns to see if certain diseases are more common in some groups
of people than others. Prostate cancer is a leading cause of cancer deaths
worldwide, but particularly in developed countries. According to figures
obtained from Globocan, a joint initiative between the International Agency
for Research on Cancer (IARC), part of WHO, and the European
Commission, New Zealand has one of the world’s highest age standardised
incidence rates at 139.06 per 100 000 people, with Australia at 108 and the
USA at 104.33. The rate for the United Kingdom is 40.24, for Italy, 24.89,
Spain, 24.23, and Greece 20.17 (International Agency for Research on
Cancer, 2000 estimates). Non modifiable risk factors include older age, family
history of the disease, and race (Giovannucci 2003). In addition, certain types
of prostate cancer appear to be associated with a diet high in red meat and
dairy products (Michaud et al. 2001). Other dietary factors may also be
important (e.g. trace elements), making it very difficult to precisely determine
critical factors relating to the disease. A recent overview of the
chemoprevention of prostate cancer details not only results relating to phase
III trials of a new pharmaceutical treatment, finasteride, but also potential
non-pharmaceutical treatments (Klein & Thompson 2004). The authors
conclude that while there is substantial evidence that selenium and vitamin E
act as preventative agents with respect to prostate cancer, there is also good
epidemiological and molecular support for lycopene, soy, green tea and
Page 18

cyclooxegenase-2 inhibitors having a similar effect. Whilst studies
undertaken to date are not unanimous in concluding a beneficial effect of
tomatoes in general, and lycopene in particular, and further research is
needed, there is strong and growing evidence of both a protective and
inhibitory effect of a diet rich in tomatoes and tomato products, with respect to
this disease. There are numerous potential reasons for why an actual
association could be missed in a study. For example, intake of tomato
products or sources of bioavailable lycopene could have been too low to be
informative.
Epidemiologic studies vary in approach. Some correlate risk of prostate
cancer with either the consumption of tomatoes and tomato products or
lycopene itself. These diet-based investigations have been either case-
control in which the diet of men prior to prostate cancer diagnosis is
compared with that of a group of cancer-free controls, or prospective, where
the diet of the sample population is measured at the beginning of the study
and the subjects followed for subsequent prostate cancer occurrence.
4.2.2 Prospective studies
An early study, considering the impact of diet and lifestyle on prostate cancer
in a population of 14 000 Adventist men, found that a higher tomato intake
was statistically significant in lowering the risk of developing prostate cancer
(Mills et al. 1989). Later, a Harvard School of Medicine study, involving 47
894 male health professionals, found that, unlike a number of other
carotenoids that had no effect, high lycopene consumption lowered the risk of
developing prostate cancer by 21% (Giovannucci et al. 1995). Furthermore,
high consumption of tomatoes and tomato products (more than 10 servings
per week) reduced the risk for all types of prostate cancer by 35%, and
advanced prostate cancer by 53%, compared with those who consumed
fewer than 1.5 servings per week. Of the tomato-based products, tomato
sauces had a high inverse association with prostate cancer risk, with a
moderate (inverse) association for fresh tomatoes and pizza and none for
tomato juice. Significantly, these gradations of association corresponded to
lycopene levels in the plasma of a sample group of the men. Of the 46 food
items analysed, tomato sauces were found to confer the greatest protection.
A recent follow up to this study, by Giovannucci et al. (2002), evaluated
additional data to see if the original associations persisted. It was concluded
that whilst frequent consumption of tomato products was associated with a
lower risk of prostate cancer, the association was only moderate and so
could be missed in a small study, a study with substantial errors in
measurement, or one based upon a single dietary assessment. In contrast, a
prospective cohort study in the Netherlands, comprising 58 279 men aged
between 55 and 69 at baseline in 1986, found no association between
lycopene, various other carotenoids, retinal, or vitamins C and E and prostate
cancer (Schuurman et al. 2002).
4.2.3 Case-control studies
One of the earliest case-control studies took place in Minnesota from 1976 to
79. In this it was also found that men with prostate cancer had a lower
reported tomato intake than men free from prostate cancer (Schuman et al.
1982), although the result was not statistically significant, possibly because
Page 19

the study was relatively small. A later case-control study in Hawaii, using a
multi ethnic population and considering the relationship between fruit and
vegetable intake and prostate cancer occurrence, found no association
between raw or cooked tomatoes and the likelihood of developing cancer (Le
Marchand et al. 1991). However, in this study actual intake levels were not
reported, nor were processed tomato products, such as tomato-based
sauces, specifically considered. Similarly, a case-control study in the United
Kingdom (Key et al. 1997) found no relationship between raw or cooked
tomatoes and the risk of prostate cancer. However, the strongest diet-related
association was found for baked beans, where the beans are generally
processed in a tomato sauce in which lycopene is present in a highly
bioavailable form. A New Zealand study during 1996-97 found that dietary
intake of lycopene and tomato-based products was only weakly associated
with a reduced risk of prostate cancer (Norrish et al. 2000). There was
approximately a 30% reduction in risk, but it was not statistically significant. In
the same study it was found that dietary intake of β-carotene and its major
vegetable sources was not protective against prostate cancer. A recent study
in China, where the prostate cancer rate is amongst the lowest in the world,
similarly found that both lycopene and consuming vegetables and fruits rich
in lycopene (as whole cooked tomatoes and watermelon) reduced the risk of
developing this disease. A protective effect of other carotenoids and
carotenoid-rich vegetables was also observed (Jian et al. 2005).
4.2.4 Clinical studies/blood and tissue studies
As mentioned earlier, lycopene has been shown to concentrate in prostate
tissues, with lycopene present in higher levels than any other carotenoid.
This has been one of the factors instigating investigation of the relationship
between lycopene and prostate cancer. Studies using levels of lycopene in
blood and/or tissue have thus investigated both the prospective and actual
incidence of prostate cancer and its virulence.
Hsing et al. (1990) used the serum taken from 25 802 people in 1974 to
compare levels of various micronutrients between those who developed
prostate cancer and those who did not. In this study lycopene was the only
carotenoid to be inversely associated with cancer risk. A study at the
University of Toronto found that levels of lycopene in serum and prostate
tissue were lower in prostate cancer patients than in cancer-free controls
(Rao et al. 1999). Gann et al. (1999) used blood samples taken and stored in
1982 when following up on the 578 cases of prostate cancer that had
occurred over the following 13 years. Comparing the baseline plasma
lycopene level with that of age-matched, cancer-free controls, it was found
that a lower risk of prostate cancer was associated with higher levels of
plasma lycopene. This was particularly evident in relation to aggressive
prostate cancer. A similar study using prediagnostic serum from Japanese
Americans in Hawaii found no association between serum lycopene levels
and risk of prostate cancer (Nomura et al. 1997). However, other researchers
have commented that flaws inherent in this study, such as the use of a single
assessment of serum lycopene to characterise a 22-year period and the
unusually low serum concentration among the controls, may account in part
for the null results (Giovannucci 2002).
Page 20

Another study, examining how prostate levels of various antioxidants related
to plasma levels and self-reported usual dietary intake, found that levels of
tocopherols and carotenoids in the prostate correlated best with respect to
lycopene, β-carotene and gamma-tocopherol (Freeman et al. 2000). In a
case-control study examining the effects of plasma lycopene and various
other antioxidants on the risk of prostate cancer, Lu et al. (2001) found
inverse associations between plasma lycopene and certain other carotenoids
and prostate cancer. A small intervention study, in which a group of 15
randomly selected patients with prostate cancer and awaiting prostatectomy
received a twice daily dose of 15 mg lycopene, found an indication that the
progression of the disease was reduced in the group under treatment
compared with the 11 controls who received no supplementation (Kucuk et
al. 2001).
Studies have investigated the higher prostate cancer rates in American
Blacks than American Whites, and found that serum lycopene levels were
significantly lower in Blacks than Whites (Hayes et al. 1999; Vogt et al. 2002).
This raised the possibility that the difference in prostate cancer rates might be
attributable to a difference in lycopene exposure. Though not statistically
significant, the results were suggestive of serum lycopene being inversely
related to risk of prostate cancer in both racial groups (Vogt et al. 2002).
Further evidence for the beneficial effects of lycopene has been
demonstrated in a number of laboratory studies. In a cell culture study,
Pastori et al. (1998) demonstrated how lycopene in combination with vitamin
E prevented the growth of prostate cancer cells. A Japanese in vitro study
investigated the effects of a number of carotenoids on three lines of human
prostate cells and found that, together with neoxanthin from spinach and
fucoxanthin from brown algae, the acyclic phytofluenes in the tomato,
including lycopene, significantly reduced the viability of these cells (Kotake-
Nara et al. 2001).
4.3 Lycopene and other cancers
In 1999 a long-time lycopene researcher, Edward Giovannucci, from the
Harvard Medical School reviewed 72 epidemiological studies regarding the
relationships between tomatoes and tomato-based products, lycopene and
cancer (Giovannucci 1999). In 57 of these studies an inverse association
between tomato intake or blood lycopene levels and the risk of several types
of cancer was shown; in 35 of these, the relationship was statistically
significant. The strongest associations were shown for the prostate and
stomach. For cancers of the lung, pancreas, colon and rectum, oesophagus,
oral mucosa, breast and cervix, the association appeared to be only
suggestive. These conclusions were consistent across diverse populations
and studies utilising various designs. None of the studies reviewed showed
evidence of increased risk of cancer from tomato/tomato-based
products/lycopene intake (Giovannucci 1999).
4.3.1 Skin cancer
Of great potential interest to New Zealanders, since skin cancer rates here
are amongst the highest in the world, are findings relating to a possible
protective effect of tomato-based products or constituent tomato
Page 21

phytochemicals. Since the role of carotenoids in plants appears to be
primarily to quench oxidative products induced by UV exposure, it is not
unreasonable to assume that lycopene could have similar activity in human
skin. An early study, considering the effects of solar-simulated light on human
skin, showed a 31-46% decrease in the lycopene of exposed skin compared
with that of adjacent non-exposed skin in a group of 16 women (Ribaya-
Mercado et al. 1995), suggesting that lycopene is actively involved in
protecting skin. A small study by Stahl et al. (2001) found that ingesting
tomato paste resulted in 40% less erythema formation at the end of a
10-week period compared with a control group. Protection against UV light-
induced erythema after regular ingestion of lycopene from tomato paste has
also been demonstrated in cell culture (Stahl & Sies 2002). Cesarini et al.
(2003), using a lycopene, β-carotene α-tocopherol and selenium mixture,
similarly showed a reduction in UV erythemas, as well as in other parameters
of epidermal defence, such as a reduction in sun burn cells, in UV-induced
p53 expression and in lipoperoxide levels. Andreassi et al. (2004) found a
lower UV-induced erythematous response in subjects applying a topical
lycopene preparation compared with those using a vitamin C and E
preparation and the control group.
In addition to skin cancer, other diseases resulting from photo-oxidative
stress induced by UV-radiation may be protected against by carotenoids such
as lycopene. These disorders include erythema formation, premature aging
of the skin, development of photodermatitis, cataract and age-related macular
degeneration (Stahl et al. 2001).
4.3.2 Cancers of the digestive tract
The various cancers of the digestive tract (oesophagus, stomach, colon and
rectum) each have individual features in terms of causation and process and
thus ideally need specific investigation. The relationship between lycopene
and cancer of the oesophagus in northern Iran was the subject of one of the
first studies to examine the role of lycopene in relation to human cancer
(Cook-Mozaffari et al. 1979). In this case-control study, weekly consumption
of tomato-based foods was associated with a 40% reduction in risk for this
cancer—a particularly prevalent cancer in this region. Similar results were
also shown much later in an Italian case-control study (Franceschi et al.
1994). A case-control study in Uruguay also showed a reduced risk of upper
aerodigestive tract (oral, pharynx, larynx and espophagus) cancers with high
tomato intake and this related to lycopene content (De Stefani et al. 2000).
With respect to stomach cancer, a number of diversely located studies have
again reported a protective effect of a tomato rich diet (Bjelke 1974; Correa et
al. 1985; Buiatti et al. 1989; Tsugane et al. 1992; Franceschi et al. 1994).
However, others have found no association (Tajima et al. 1985; Ramon et al.
1993). Another study examined the possible relationship between levels of
lycopene, α-carotene and β-carotene in the gastric mucosa and the presence
of Helicobacter pylori, a pathogen thought to provoke an inflammatory
response that precipitates the train of events leading to the development of
gastric cancer. No difference in the levels of these carotenoids was found
between H. pylori-infected subjects and controls (Sanderson et al. 1997).
Page 22

Cancers of the colon and rectum are major health problems in developed
countries and have been consistently found to be inversely associated with
high dietary intakes of fruits and vegetables. Whilst there are many studies in
which tomatoes have not been specifically considered, a number have
reported an inverse relationship between the intake of tomatoes and tomato-
based products and these health problems (Modan et al. 1981; Maquart-
Moulin et al. 1986; Benito et al. 1990). However, a Canadian prospective
cohort study of carotenoids (including lycopene) and colorectal cancer risk
did not support any association (Terry et al. 2002).
In vitro effects have also been reported for these types of cancer. Lycopene
has been shown to inhibit cell proliferation and enhance gap-junction
communication in human oral tumour cells (Livny et al. 2002).
Antiproliferative effects have also been shown against other digestive
cancers (Velmurugan et al. 2002).
4.3.3 Breast cancer
There have been mixed results with respect to the association between
lycopene intake and breast cancer. No association was found in studies in
the early 1990s by Potischman et al. (1990), London et al. (1992), and
Garland et al. (1993), looking at potentially protective effects of carotenoids
and antioxidants. A Finnish study of 4697 women equally showed no
relationship between consumption of tomato-based products and the risk of
developing breast cancer (Jarvinen et al. 1997). More recent Italian (La
Vecchia 2002) and Canadian (Terry et al. 2002) studies also showed no
consistent association for lycopene and breast cancer. Samples from the
Breast Cancer Serum Bank in Missouri were analysed for levels of
carotenoids, selenium and retinal, with only lycopene being found to be
related to a reduced risk of developing breast cancer (Dorgan et al. 1998). A
recent case-control Swiss study investigating the relationship between 17
micronutrients and breast cancer found that lycopene was significantly
inversely associated with breast cancer risk (Levi et al. 2001).
Various mechanisms of action against breast cancer have been
demonstrated in animal studies or in vitro. In a Boston study using induced
mammary cancers in a population of rats, it was found that an injection of
lycopene-enriched tomato oleoresin appeared to correlate with fewer and
smaller tumours in treated animals than in those who were treated either with
β-carotene or who were untreated (Zhang et al. 1997). Similarly, another
study (Nagasawa et al. 1995) showed that spontaneous mammary tumours
were inhibited in mice fed a lycopene-rich diet. Using cell-cultured human
mammary cancer cells a 1995 study reported lycopene-inhibited proliferation,
whereas other carotenoids, β- and α-carotene, were less effective (Levy et al.
1995).
4.3.4 Ovarian and cervical cancer
A number of studies have also investigated the role of lycopene in preventing
ovarian and cervical cancers. A recent population based study of pre- and
post-menopausal women found that in both groups lycopene intake was
significantly inversely associated with ovarian cancer (Cramer et al. 2001). Of
the foods investigated, for raw carrots and tomato ketchup the (inverse)
Page 23

association was strongest. Examining the role of various micronutrients and
in the development of cervical cancer, a 1998 study found that of a number of
micronutrients, only lycopene was lower in cancer patients than in the
controls (Goodman et al. 1998). Similarly, Sengupta & Das (1999) found that
higher levels of lycopene were inversely associated with risk, and Kanetsky
et al. (1998) found that among black, non-Hispanic women, the risk of
developing cervical cancer was reduced by 33% in women with higher blood
levels of lycopene. However, again there have been other studies in which no
evidence was found between either lycopene intake or serum concentrations
and risk (Potischman et al. 1991, 1994; Batieha et al. 1993).
4.3.5 Bladder cancer
As with many other cancers, it has been found that a diet rich in fruit and
vegetables is associated too with a protective role against bladder cancer
(Block et al. 1992). Looking at tomatoes, lycopene and other micronutrients
with respect to bladder cancer risk, Helzlsour et al. (1989) found an inverse
association only with lycopene and selenium concentrations. Conversely,
however, a laboratory study of induced bladder tumours in mice showed a
mild but statistically non significant effect of lycopene or β-carotene on the
number of transitional cell carcinomas (Okajima et al. 1997).
4.3.6 Lung cancer
To date, studies considering the relationship between lycopene and lung
cancer have not shown strong effects. Holick et al. (2002) found that a diet
rich in carotenoids, including tomatoes and tomato-based products, might
reduce the risk of cancer. Similarly an English study found that together with
fish liver oil, vitamin pills and carrots, tomato juice decreased the risk of
contracting lung cancer in a case-control study of smokers (Darby et al.
2001). Kim et al. (2000) found that lycopene inhibited the development of
carcinogenises in the lungs of male, but not female mice. Hecht et al. (1999)
found that administration of lycopene-enriched tomato oleoresin had no effect
on the development of induced lung tumours in mice.
4.4 Cardiovascular disease
Cardiovascular disease (CD) is the leading cause of illness and death in most
developed countries. It includes myocardial infarction (heart attack),
ischaemic heart disease (narrowing of the arteries) and cerebrovascular
disease (stroke), and has been estimated to be responsible for around 40%
of deaths in Australasia (Lister 2003). Whilst certain strategies can be
adopted to reduce risk factors for this health problem, such as maintaining a
healthy body weight, eliminating cigarette smoking and taking more physical
exercise, evidence has now accumulated to suggest that dietary factors may
also be important. Just as the Mediterranean diet is believed to prevent
various cancers, so too is it believed to protect against cardiovascular
problems.
The free radicals responsible for initiating the oxidative damage that lead to
cancer are also believed to be responsible for the oxidation of the low density
lipoproteins (LDL) that carry cholesterol in the bloodstream. Evidence
increasingly supports the hypothesis that oxidatively damaged
Page 24

macromolecules derived from the lipoproteins that have been deposited on
the blood vessel wall may initiate the cellular and cytokine networks involved
in the development of vessel lesions (Ross 1993). This is an early stage in
the development of the atherosclerosis that precedes wider cardiovascular
health problems. Thus, antioxidant nutrients may retard the progression of
this disease by interfering with the oxidative process. In addition, however,
mechanisms besides lycopene’s antioxidant properties have been shown to
reduce the risk of CD. In a small clinical trial and laboratory experiment it was
demonstrated by Fuhrman et al. (1997) that lycopene inhibited the activity of
a particular enzyme involved in cholesterol synthesis. It has been
hypothesised that other activity could include enhanced LDL degradation,
LDL particle size, and composition, plaque rupture and altered endothelial
functions (Rao 2002).
In the past, many studies have credited the antioxidant activity of vitamin E
for providing a protective effect against lipid oxidation (Rimm et al. 1993;
Morris et al. 1994). However, this was not confirmed in the Heart Outcomes
Prevention Evaluation Study in the United States, which found no evidence of
beneficial effects in cardiovascular terms for high risk patients (Hoogwerf &
Young 2000). However, other studies specifically examining the effects of
consuming tomatoes and tomato products found a decreased risk of CD with
intake of these foods. In a multi-centre case-control study, with subjects
recruited from 10 European countries, the relationship between antioxidant
status and acute myocardial infarction was evaluated. Adipose tissue
samples were taken from subjects directly after the infarction and analysed
for various carotenoids. These were then compared with matched controls.
After statistical adjustment for potentially confounding variables, the only
carotenoid that showed a protective effect was lycopene (Kohlmeier et al.
1997). In a small intervention study, Argawal & Rao (1998) examined the
effects of various forms of lycopene (tomato juice, spaghetti sauce and
tomato oleoresin soft gel capsules) that were added to the diet of the 19
subjects for a period of one week each. All treatments resulted in higher
levels of serum lycopene and significantly decreased LDL oxidation and
serum lipid peroxidation, but had no effect upon cholesterol levels. In contrast
with the latter finding, a study investigating cholesterol metabolism using cell
culture and a small clinical trial found that, firstly, incubation of human
macrophage cells with lycopene inhibited cholesterol synthesis and
augmented macrophage LDL receptors and that, secondly, dietary
supplementation of 60 mg lycopene daily in six males over the course of
three months resulted in a 14% reduction in plasma LDL cholesterol levels
(Elinder et al. 1995). In a study comparing Lithuanian and Swedish men from
populations with differing mortality rates from coronary artery disease, it was
also found that lower blood lycopene levels were associated with a higher
risk of both developing and dying from the disease (Kristenson et al. 1997).
The findings of a Finnish study (Rissanen et al. 2003) found greater
thickening of the wall of the common carotid artery in men with lower serum
lycopene concentrations than in men with higher than median lycopene
plasma, although the difference for women was not significant. A second
study, by the same group, found that men in the lowest quartile of serum
levels of lycopene had a 3.3 fold higher risk of an acute coronary event or
stroke than the others.
Page 25

4.5 AIDS
Many studies have observed reduced levels of micronutrients in HIV patients,
despite dietary intakes that would normally be considered adequate. Lower
concentrations of serum lycopene were recorded in HIV-positive women
(Coodley et al. 1995), and children (Periquet et al. 1995). It has been
postulated that this may result from the problem of lipid malabsorption, a
common feature of progressive HIV disease (Clinton 1998).
4.6 Diabetes
Type 2 diabetes, in which the body is unable to utilise insulin, is another
chronic disease associated with the oxidation of LDL. It is a disease in which,
amongst other health outcomes, there is frequently an increased risk of CD. It
has been found in vitro that high levels of glucose, as present in Type 2
diabetes, increase LDL oxidation (Bierman 1991) and that glycated LDL is
particularly prone to oxidation (Semenkovich & Heinecke 1997). Also,
diabetic subjects have increased levels of small, dense, LDL which is more
readily oxidised than larger LDL (Semenkovich & Heinecke 1997), as well as
elevated levels of certain biological markers that suggest stimulation of the
inflammatory activity that increases the risk of coronary events (Libby &
Ridker 1999). Data analysed form the Third National and Nutrition
Examination Survey in the United States found significantly lower levels of
lycopene in subjects with impaired glucose tolerance and levels that were
lower again in newly diagnosed diabetic patients than in controls with normal
glucose tolerance (Ford et al. 1999). Similarly, diabetic Asian Indian
physicians living in the USA were found to have lower levels of lycopene than
non-diabetic counterparts (Chuang et al. 1998), as did elderly Type 2
subjects in an Italian study (Polidori et al. 2000). In a recent New Zealand
clinical trial, involving supplementation with two cups of tomato juice daily in a
group of Type 2 diabetic patients, it was found that plasma levels of lycopene
markedly increased and that the resistance of localised LDL to oxidation also
increased (Upritchard et al. 2000).
4.7 Eye disease
Some carotenoids, such as lutein and zeaxanthin, are well known to play an
important role in eye health (Meltzer & Kravets 1998). Less is known about
the potential role of lycopene. High concentrations have been reported in
certain parts of the eye (ciliary body and retinal pigment epithelium) and so
may have some function in protecting against age-related macular
degeneration (AMD) and other eye diseases (Khachik et al. 2002). In a
population-based, case-controlled study regarding the relationship of AMD
and carotenoid levels it was found that individuals with low serum levels of
lycopene were twice as likely to have AMD as those with higher serum levels
(Mares-Perlman et al. 1995). An Australian study, however, found no
evidence of protective effects of lycopene and other antioxidants on the early
(within five years) age-related maculopathy (Flood et al. 2002).
Page 26

A study with rats showed lycopene to have an inhibitory effect on cataract
development (Pollack et al. 1996). Lycopene has also been shown to offer
protection against galactose-induced cataract changes in lens tissue (Trivedi
et al. 2001a) and be protective against selenite-induced stress (Trivedi et al.
2001b).
5 The role of other tomato
components in human health
There has been less specific study of the importance of other tomato
components on human health, although the groups of compounds
themselves have been studied.
5.1 Other carotenoids
Although the above studies have largely focused on lycopene, other
carotenoids in tomatoes are likely to contribute to their health benefits. Other
carotenoids may have similar effects to lycopene, although some health
benefits do seem to be specific to lycopene. Lycopene does have stronger
antioxidant activity than many other carotenoids, such as β-carotene (Di
Mascio et al. 1989). However, some other carotenoids play important
physiological functions that lycopene does not. Those carotenoids with at
least one unsubstituted β-ring and an unchanged side change (e.g. β-
carotene, α-carotene, cryptoxanthin, γ-carotene) may be converted to vitamin
A in the body. Such carotenoids are referred to as having provitamin A
activity. Because lycopene does not have the ring structure it cannot be
converted to vitamin A.
As with lycopene, most other carotenoids are being considered as potential
cancer prevention agents, although there have been mixed results in trials.
Studies of β-carotene indicate that its benefits may only occur when it is
derived from food and not when it originates from a supplement form. β-
Carotene has been used as a so-called oral sun protectant due to its
antioxidant properties, and its efficacy has been shown in human studies
(Stahl et al. 2000). However, these studies were not with tomatoes. It is
unlikely that the level of β-carotene in tomatoes is high enough, alone, to
offer this level of protection.
Another group of carotenoids, the xanthophylls (e.g. lutein and zeaxanthin),
have specific distribution patterns in human tissue, especially in the retina of
the eye (Zaripheh & Erdman 2002). These carotenoids are thought to be
important for normal eye function and play a role in the prevention of various
eye diseases, including macular degeneration, glaucoma and cataracts
(Head 1999, 2001).
Page 27

5.2 Phenolic compounds
The considerable diversity of the structure of phenolics makes them different
from other antioxidants. Several thousands of natural polyphenols have been
identified in plants, many of them in plant foods (Shahidi & Naczk 1995),
although only a more limited number are at significant levels in most human
diets. The chemical structure of polyphenols affects their biological properties:
bioavailability, antioxidant activity, specific interactions with cell receptors and
enzymes, and other properties. There has been little specific study of the role
that tomato flavonoids, and other phenolics, may play in human health.
However, this group of compounds has received considerable attention, in
general, but particularly those compounds in red wine, tea, chocolate and
onions.
Phenolic compounds, because of their structure, are very efficient
scavengers of free radicals and they also serve as metal chelators (Shahidi &
Naczk 1995). In addition to their antioxidant characteristics, other potential
health-promoting bioactivities of the flavonoids include anti-allergic, anti-
inflammatory, anti-microbial and anti-cancer properties (Cody et al. 1986;
Harbourne 1993). There are many ways in which flavonoids may act to
prevent cancer, including inducing detoxification enzymes, inhibiting cancer
cell proliferation and promoting cell differentiation (Kalt 2001). Some
flavonoids are also beneficial against heart disease because they inhibit
blood platelet aggregation and provide antioxidant protection to LDL (Frankel
et al. 1993). Studies on the health benefits of the phenolic acids to date have
largely focused on their antioxidant activity.
5.3 Other
Research at the Rowett Research Institute in Scotland has identified a
component in the yellow jelly around tomato seeds that, it is proposed, stops
platelet cells in the blood from clumping together (Dutta-Roy et al. 2001). The
aggregation of platelets triggers the cascade of reactions leading to blood clot
formation (thrombosis). Heart attacks, strokes and blood vessel problems
resulting from thrombosis currently kill or disable more people in developed
countries than any other disease. In tests on volunteers, the compound
(codenamed P3) from as few as four tomatoes reduced platelet activity by up
to 72%. Larger scale studies are necessary to confirm these results but, if
successful, P3 could represent a benefit over existing anti-platelet therapy,
such as aspirin, which may have side effects such as stomach upsets and
bleeding (Dutta-Roy et al. 2001). A Japanese study in 2003 tested various
tomato cultivars in relation to anti-thrombotic effects using both in vitro and in
vivo (rat model) methods. One variety showed not only significant anti-
thrombotic activity with both methods, but also inhibited thrombus formation
as well as having a thrombolytic effect (Yamamoto et al. 2003).
Page 28

6 Bioavailability of tomato
phytochemicals
6.1 Lycopene
A correlation between seven-day food diary lycopene intake and plasma
lycopene has been noted (Forman et al. 1993). In contrast it has been found
that there is no correlation between plasma lycopene and high fruit and
vegetable intake (Campbell et al. 1994). This may be because lycopene only
comes from one major food source (tomatoes and tomato products) and a
high fruit and vegetable intake may not imply a high lycopene (tomato) intake.
It has been shown that plasma lycopene can be increased in a relatively
short time by increasing the dietary intake of this carotenoid (Johnson 1998).
It has been demonstrated that dietary lycopene is absorbed and distributed in
humans. Its bioavailability depends on various factors such as food
processing and co-ingestion of fat (Sies & Stahl 1999). Since lycopene is a
fat-soluble compound, it follows the same intestinal absorption path as
dietary fat. Absorption is influenced by the same factors that influence fat
absorption. Thus, the absence of bile or any generalised malfunction of the
lipid absorption system will interfere with the absorption of lycopene.
Lycopene is released from food matrices and solubilised in the gut. This is
done in the presence of fat and conjugated bile acids. The efficiency of
release is influenced by such factors as disposition of lycopene in the food
matrix, particle size after mastication and stomach action, and the efficiency
of digestive enzymes (Johnson 1998). Heating of plant foods before ingestion
improves the bioavailability of lycopene, partly because protein-carotenoid
complexes are weakened (Stahl & Sies 1992).
After absorption into the intestinal musosa, lycopene is transported in the
plasma exclusively by lipoproteins (Johnson 1998). Lycopene appears first in
the very low density lipoprotein (VLDL) and chylomicron fractions of plasma
and later in low density lipoprotein (LDL) and high density liipoprotein (HDL),
with highest concentrations in the LDL (Krinsky et al. 1958). The distribution
of lycopene among lipoproteins is similar to β-carotene and similar between
men and women (Forman et al. 1998; Reddy et al. 1989). Serum
concentrations can vary substantially (50 to 900 nM), both within the
individual and between individuals (Bramley 2000). It is hydrophobic and is,
therefore, generally located within cell membranes. Although lycopene is
found in most human tissues, it is not distributed evenly, with substantially
larger amounts found in the adrenals and testes (Table 10).
Page 29

Table 10: Lycopene levels in human tissues
(Bramley 2000 - data taken from Schmitz et al.
1991; Stahl et al. 1992; Clinton et al. 1996).
Tissue Lycopene (nmol/g wet weight)
Adipose 0.2-1.3
Adrenal 1.9-21.6
Brainstem nda
Breast 0.8
Colon 0.3
Liver 1.3-5.7
Lung 0.2-0.6
Ovary 0.3
Prostate 0.8
Skin 0.4
Stomach 0.2
Testis 4.3-21.4
a Not detected.
Cis-isomers of lycopene make up >50% of the total lycopene in human
serum and tissues (Stahl et al. 1992; Clinton et al. 1996). This is in contrast
to the food sources from which they originate; in tomatoes and tomato-based
food products all trans-lycopene comprises 79-91% of total lycopene (Clinton
et al. 1996). Stahl & Sies (1992) studied the uptake of lycopene and its
geometrical isomers from heat-processed and unprocessed tomato juice in
humans. Lycopene concentrations in human serum increased only when
processed tomato juice was consumed. Lycopene uptake varied with
individuals, but peak serum concentrations were always reached between 24
and 48 hours. The carotenoid was eliminated from serum with a half-life of
two to three days. The increase in peak serum concentrations was dose-
dependent but not linear with the dose. Repeated doses led to a continual
rise of lycopene in human serum. Of the different geometrical isomers (all-
trans, 9-cis and 13-cis), the cis-isomers seemed to be somewhat better
absorbed than the all-trans form. More detailed studies with ferrets have
shown that the cis-isomers of lycopene are more bioavailable than trans-
lycopene, probably because they are more soluble in bile acid micelles and
may be preferentially incorporated into chylomicrons (Boileau et al. 1999).
In addition to examining the effect of heat treatment, van het Hof et al. (2000)
looked at the effects of the degree of homogenisation on the bioavailability of
lycopene. Both additional heat treatment (one hour at 100°C, compared to
just heating before serving) and homogenisation increased carotenoid
(lycopene and β-carotene) bioavailability from tomatoes (canned, so already
had heat treatment during manufacture), although the effect of additional
heating was not always significant. Disruption of the tomato matrix also
enhanced the ease with which carotenoids could be extracted from the
Page 30

tomatoes. Homogenisation and heat treatment disrupt cell membranes,
enhancing extractability, and heat treatment has also been suggested to
disrupt further the protein-carotenoid complexes. Homogenisation under high
pressure was more effective in increasing carotenoid bioavailability than
homogenisation under normal pressure. Thus, the release of carotenoids
from cells is a limiting factor in bioavailability.
The bioavailability of lycopene from fresh tomatoes versus tomato paste was
compared in human volunteers (Gärtner et al. 1997). The lycopene intake
from both the fresh tomatoes or the tomato paste was 23 mg and the meals
were ingested together with 15 g of corn oil. The lycopene isomer pattern
was the same in both cases. Ingestion of tomato paste yielded much higher
peak concentrations and under the curve responses for all-trans lycopene
and its cis-isomers. No difference was observed for the α- and β-carotene
response. Porrini et al. (1998) also reported that lycopene from tomato puree
(16.5 mg/day) resulted in significantly higher plasma concentrations than
fresh tomatoes. Thus, in humans the bioavailability of lycopene is higher from
processed tomato products than fresh tomatoes, independent of the doses.
Lycopene serum concentrations increased significantly after ingestion of 39-
75 mg/day lycopene from spaghetti sauce, tomato juice and lycopene
capsules (Rock & Swendseid 1992). This study did not indicate any
significant differences in absorption between the differing food matrices.
Lycopene absorption from supplements (oleoresin capsules) and from
processed tomato products were comparable (Bohm & Bitsch 1999).
It has further been noted that absorption of carotenoids, including lycopene,
is improved when consumed in conjunction with dietary lipids (Bohm & Bitsch
1999). It has been proposed that high-dose intake of a particular carotenoid
may antagonise the bioavailability and absorption of other carotenoids.
However, one study found that ingestion of a combined dose of β-carotene
and lycopene had little effect on the absorption of β-carotene but improved
that of lycopene (Johnson et al. 1997). A recent study investigated possible
interactions between the transport of β-carotene and lycopene and found that
they may compete for the same transport mechanism (Gaziano et al. 1995).
When extremely high doses of β-carotene were fed to humans compared to
the magnitude of β-carotene uptake into LDL, the concentration of lycopene
in LDL reduced. However, the doses fed were well beyond those achieved in
a healthy diet.
There are a range of physiologic factors that influence plasma concentrations
of carotenoids. For example, for β-carotene plasma concentrations are higher
in women than men, although for lycopene there appears to be no sex
difference in its absorption or utilisation. Increasing age has been found to be
inversely related to plasma lycopene (Brady et al. 1996). One explanation for
this observation is that younger individuals consume more of some lycopene-
rich foods such as pizza and ketchup. However, it would appear to only
partially explain the difference (Johnson 1998). Smoking is well known to
decrease plasma β-carotene levels but lycopene seems to be affected to a
lesser extent (Johnson 1998). Alcohol intake appears not to affect plasma
lycopene levels (LeComte et al. 1994; Forman et al. 1995).
Page 31

A lycopene formulation where lycopene was entrapped with whey proteins
(named “lactolycopene”) was shown to be as bioavailable as lycopene from
processed tomatoes (Richelle et al. 2002).
6.2 Other carotenoids
The bioavailability of some other carotenoids, especially β-carotene, has
been well demonstrated from a variety of fruit, vegetable and supplement
sources (Castenmiller & West 1998; van het Hof et al. 2000; Yeum & Russell
2002; Zaripheh & Erdman 2002). As noted with lycopene, various dietary
factors have an effect on the bioavailability of carotenoids (Table 11). The
type of food matrix in which carotenoids are located is a major factor. The
bioavailability of β-carotene from vegetables in particular has been shown to
be low (14% from mixed vegetables) compared to when purified β-carotene is
added to a simple matrix (e.g. salad dressing), whereas for lutein, the
difference is much smaller (relative bioavailability of 67% from mixed
vegetables). Processing, such as mechanical homogenisation or heat
treatment, has the potential to enhance the bioavailability of carotenoids from
vegetables (from 18 to nearly 120%). The amount of dietary fat required to
ensure carotenoid absorption is moderate (~3–5 g per meal), although it
depends on the physicochemical characteristics of the carotenoids ingested,
but the presence of fat is important. Unabsorbable, fat-soluble compounds
reduce carotenoid absorption, and interaction among carotenoids may also
result in a reduced carotenoid bioavailability.
Table 11: Estimation of the quantitative effects of various dietary factors on the bioavailability of
carotenoidsa (from van het Hof et al. 2000).
Carotenoid
Dietary factor nbβ-Carotene Lutein Lycopene
Matrix type (carotenoids in oil = 1.0)
Mixed vegetables 10–22 0.14 ± 0.011 0.67 ± 0.08 nac
Green leafy vegetables 56–62 0.04 nacnac
Whole-leaf spinach 10–12 0.04 0.45 nac
Whole-leaf spinach 26–67 0.03 ± 0.5 nacnac
Carrots 7–15 0.19 nacnac
Carrots 5 0.19 nacnac
Carrots 12–13 0.26 nacnac
Broccoli 5 0.22 nacnac
Broccoli 26–67 0.74 ± 0.64 nacnac
Green peas 26–67 0.96 ± 0.71 nacnac
Matrix disruption (undisrupted vegetables = 1.0)
Chopped v. whole-leaf spinach 26 1.0 1.18 nac
Liquefied v. whole-leaf spinach 12 1.69 1.0 nac
Homogenized v. whole carrots 13 [1.7]dnacnac
Homogenized v. whole carrots 7–10 5.9 nacnac
Page 32

Carotenoid
Dietary factor nbβ-Carotene Lutein Lycopene
Tomato paste v. raw tomatoes 5 nacnacnac
Tomato paste v. raw tomatoes 9 nacnac1.2–1.5
Homogenized and heated v. raw
carrots and spinach
8 3.1 nacnac
Amount of dietary fat (high amount of fat = 1.0)
0 g fat v. 5 g fat present in
carotenoid-supplemented meal
22–26 0.48fnacnac
0 g fat v. 10 g fat present in
carotenoid-supplemented meal
22–26 0.48gnacnac
5 g fat v. 10 g fat present in
carotenoid-supplemented meal
22 1.0 nacnac
3 g fat v. 18 g fat present in meal
containing sweet potatoes
41–43 0.63fnacnac
3 g fat v. 36 g fat present in
carotenoid-supplemented meal
15 1.0 0.43 ±
0.062g
nac
Indigestible fat-soluble compounds (regular dietary fat = 1.0)
3 g/d sucrose polyester v. regular
dietary fat with main meal
26–27 0.80 ± 0.03 nac0.62 ± 0.05
12.4 g/d sucrose polyester v. regular
dietary fat with main meal
21 0.66 ± 0.02 0.80 ± 0.04 0.48 ± 0.05
18 g/d sucrose polyester v. regular
dietary fat at v.arious times during
day
65–67 0.73 0.81 0.77
Dietary fibre (no dietary fibre = 1.0)
12 g/d citrus pectin added to
carotenoid-supplemented meal
7 0.42 na na
Beet root fibre added to liquefied
spinach
12 1.0 1.0 na
a Values are presented as means ± SEM or as mean. The factors were calculated from changes in plasma or serum
concentrations of carotenoids, unless otherwise stated. The plasma or serum carotenoid response after the treatment
stated was divided by the plasma or serum carotenoid response after the treatment, which was taken as a reference at
1.0 (identified between brackets for each dietary factor), and corrected if necessary for differences in carotenoid intake.
In case no change was expected from the reference treatment (e.g. in case of indigestible v. regular fat), the factors
were calculated as the percentage of change from baseline, corrected if necessary for the change in the control group.
A factor <1.0 indicates that the bioavailability of carotenoids is reduced compared with the reference chosen; a factor
>1.0 indicates an enhanced carotenoid bioavailability.
b Number of subjects per treatment.
c Not assessed.
d Value is not significantly different from 1.0 (α= 0.05).
e Calculated from area under the curve of the carotenoid response in triglyceride-rich lipoproteins.
f Calculated from changes in serum concentrations of retinol.
g Lutein was present as lutein esters.
Page 33

There are few xanthophylls (e.g. lutein) in tomatoes but they are an important
group of carotenoids. The xanthophylls, lutein and zeaxanthin, have specific
distribution patterns in human tissue, especially in the retina of the eye
(Zaripheh & Erdman 2002). The presence of these xanthophylls is thought to
provide protection from macular degeneration. Like other carotenoids,
environmental factors, food processing, food matrix, structural differences and
the interaction among other food components all have an effect on their
efficiency of uptake and absorption. From the limited human studies
described in the literature, lutein appears to be more bioavailable from food
sources than does β-carotene (Zaripheh & Erdman 2002). The disruption of
the food matrix seems to improve β-carotene’s bioavailability more than that
of lutein. There is no evidence that a negative interaction between
carotenoids occurs when foods are ingesting. However, interactions do occur
between xanthophylls and carotenes when supplements are consumed.
Several studies found that when they were consumed simultaneously, β-
carotene reduced lutein bioavailability. With the broad consumption of lutein
supplements from marigold flowers, some of which are high in lutein diesters,
the question of lutein diester bioavailability arises. More dietary fat seems to
be required for efficient absorption of lutein from lutein diester sources.
Despite these studies there are limited data on the bioavailability of
carotenoids other than lycopene from tomatoes. Studies examining the
bioavailability of lycopene have also demonstrated that β-carotene, and some
other carotenoids, from tomatoes are bioavailable (Richelle et al. 2002; van
het Hof et al. 2000), although these data are quite limited. Phytofluene has
been shown to be better absorbed than lycopene from tomatoes (Richelle et
al. 2002).
6.3 Phenolics
There have been various studies of the bioavailability of different phenolics
(reviews by Rice-Evans et al. 2000; Ross & Kasum 2002; Scalbert &
Williamson 2000). Phenolic acids account for about one-third of the total
dietary phenols and flavonoids account for the remaining two-thirds (Scalbert
& Williamson 2000). A total intake of polyphenolics of ~1 g/d was suggested
over 25 years ago (Kühnau 1976). However, large uncertainties in the
polyphenol intake and in the variations of intake remain. Comprehensive
surveys on the content of some important polyphenol classes (e.g.
anthocyanins, proanthocyanidins, phenolic acids) are still lacking. The
intestinal absorption of polyphenols can be high, but differs markedly
between the different groups (Table 12). Some flavonol glycosides are better
absorbed than their aglycones, but very little is known about the influence of
other structural parameters. However, the plasma concentration of any
individual molecule rarely exceeds 1 µM after the consumption of 10–100 mg
of a single compound. Measurement of the plasma antioxidant capacity
suggests that more phenolic compounds are present, largely in the form of
unknown metabolites, produced either in our tissues or by the colonic
microflora. Further research is required in this area.
Page 34

Table 12: Bioavailability in humans of polyphenols consumed alone or in foodsa (taken from Scalbert
& Williamson 2000).
Polyphenol Source
Quantity of
polyphenol
ingested
(mg)
Maximum
concentration
in plasma
(µM)
Excretion
in urine
(%)
Phenolic acids
Caffeic acid 1000 27
Flavonols
Quercetin Onion 68 0.74 1.39
Quercetin Apple 98 0.30 0.44
Quercetin-4-O-
rhamnoglucoside
Pure compound 202 0.30 0.35
Quercetin-4-O-glucoside Pure compound 144 3.2
Quercetin Onion 139 1.34 0.8
Quercetin Mixed black currant and apple
juice, 1000 ml/d for 7 d
6.4 0.5
Catechins
Epigallocatechin gallate Green tea infusion, 1.2 g 88 0.33 ndb
Epigallocatechin 82 0.67 3.6
Epicatechin gallate 33 ndbndb
Epicatechin 32 0.27 6.2
Epigallocatechin gallate Green tea infusion, 5 g 105 0.13–0.31
Epigallocatechin gallate Green tea infusion, 6 g 5.0
Epigallocatechin gallate Green tea extract 525 4.4
Catechin Red wine, 120 ml 34 0.072
Catechin Pure compound 500 2.0 0.45
Isoflavones
Genistein Soy milk 19 0.74 19.8
Daidzein 25 0.79 5.3
Genistein Soy proteins, 60 g/d for 1 mo 20 9.2
Daidzein 25 2.5
Genistein Soy proteins, 60 g/d for 28 d 80 0.50
Daidzein 36 0.91
Genistein Soy proteins, 20 g/d for 9 d 23 8.7
Daidzein 13 26
Flavanones
Naringin Grapefruit juice, 120 m 43 <4 8.8
Naringin Grapefruit and orange juice,
1250 ml each
689 6.8
Hesperidin 89 24.4
Naringin Pure compounds 500 4.9
Hesperidin 500 3.0
Anthocyanins
Anthocyanins Red wine, 300 ml 218 1.0–6.7
a Polyphenols, principally in the form of conjugated metabolites, as sulfate esters or glucuronides, in plasma and urine,
were hydrolysed by acid or enzymes before chromatrographic or colorimetric analysis.
b Not detected.
Page 35

Only one study was found that looked specifically at the bioavailability of
tomato phenolics. Naringenin from cooked tomato paste has been shown to
be bioavailable in men (Bugianesi et al. 2002). Although rutin and chlorogenic
acid were detected in the tomato paste used in this study they were not
detected is plasma after tomato paste consumption. The levels of many of
the phenolics in tomato may not be sufficiently high enough to be picked up
in plasma in bioavailability studies using current methodology. Although there
has only been one specific study on the bioavailability of phenolics from
tomatoes, some of the compounds present have been shown to be
bioavailable from other foods. Rutin has been shown to be bioavailable,
although less so than some other quercetin glycosides or the aglycone
(Erlund et al. 2001; Graefe et al. 2001). In one study examining quercetin and
rutin, they were found in plasma as glucuronides and/or sulfates of quercetin
and as unconjugated quercetin aglycone, but no unchanged rutin was
detected (Erlund et al. 2000). Other studies on the bioavailability of phenolic
acids have demonstrated that coumaric acid, from coffee and blackcurrant
juice, was bioavailable (Nardini et al. 2002; Rechner et al. 2002). However,
for coffee although chlorogenic acid was present in high amounts it was not
detected in plasma (Nardini et al. 2002). It is possible that it is metabolised to
other compounds, which may or may not have biological activity.
7 Tomato/lycopene consumption and
major disease patterns
As discussed earlier, epidemiologic studies (also called observational or
population studies) look at disease patterns to see if certain diseases are
more common in some groups of people than others. By examining these
data together with dietary information, patterns can be identified as to the
influence of protective components from the diet. Table 13 shows the
incidence of certain diseases in New Zealand populations compared to some
other selected countries.
Not surprisingly, there is no official recommended daily intake for tomatoes or
tomato products or their constituent compounds. More research is needed to
identify the active compounds and establish the full health benefits derived
from tomatoes. Researchers to date, who have largely been concerned with
investigating the benefits of lycopene and have considered optimum intake
levels, vary somewhat in what they consider to be necessary to have an
efficacious effect. After considering results from the Health Professionals
Follow-Up Study, Giovannucci suggests that two to four servings of tomato
sauce per week (not ketchup) reduce the risk of prostate cancer by one-third
to one-half (Giovannucci et al. 1995; Giovannucci 2003). Yeung and Rao in
their book, ‘Unlock the power of lycopene’, recommend at least one serving
of processed tomato daily. Other researchers mention a recommended intake
of 35 mg of lycopene daily (Rao & Agarwal 2000), but this may be rather
high. Roughly estimated, this amount could be obtained, for example, from
two glasses of tomato juice (500 ml) or through a combination of tomatoes
and tomato products (e.g. pasta sauce, fresh tomatoes).
Page 36

Carotenoid intake has been estimated from food frequency questionnaires. In
Great Britain the daily consumption of lycopene-rich food was equivalent to a
lycopene intake of about 1.1 mg per day (Scott et al. 1996). In a study from
the United States a daily intake of about 3.7 mg per day was reported
(Forman et al. 1993). However, another study (Rao & Agarwal 1998)
estimated it to be 25 mg/day, with processed tomato products accounting for
50% of the total intake (Table 14). This figure seems incredibly high and
unlikely to be achieved by many people. Even Mediterranean diets may not
achieve these levels. No such specific data have been reported for New
Zealand and Australian populations.
Table 13: Prostate cancer incidence and mortality and mortalities from
major cardiovascular diseases in some Mediterranean and non-
Mediterranean countries.
Disease rates per
100 000 NZ USA Italy Spain Greece UK
Prostate cancer cases
(age standardised)1
139.1 104.3 24.9 24.2 20.2 40.2
Prostate cancer
mortalities (age
standardised)1
21.2 17.9 12.1 15.0 10.7 18.5
Diseases of circulatory
system mortalities2
343.6 362.0 302.9 272.5 382.5 363.8
Ischaemic heart disease
mortalities2
199.9 181.1 103.3 90.9 117.7 209.6
Acute myocardial
infarction mortalities2
98.4 84.9 54.6 62.2 88.6 114.3
Cerebrovascular disease
mortalities2
68.9 55.7 80.4 73.4 127.0 81.0
Sources of data:
1. Globocan 2000 estimates Figures age standardised according to Segi’s world population.
2. Global Cardiovascular Infobase 1997 age standardised death rates are generated using
the world standard population based on J. Waterhouse et al. (ed). Cancer incidence in five
continents, Lyon, IARC, 1976 (Vol. 3, pl 456), as used by WHO.
Age-standardised data: An age-standardised rate (ASR) is a summary measure of a rate
that a population would have if it had a standard age structure. Standardisation is
necessary when comparing several populations that differ with respect to age because age
has such a powerful influence on the risk of cancer. The most frequently used standard
population is the World standard population. The calculated incidence or mortality rate is
then called World Standardised incidence or mortality rate. It is also expressed per 100 000
(from Globocan).
Page 37

Table 14: Estimates of daily intake of lycopene from tomatoes and tomato
products, as determined from a food-frequency questionnaire (from Rao
et al. 1998).
Product Serving size
Lycopene intake
(mg/d per subject)
% of total daily
lycopene intake
Tomatoes 200 g 12.70 50.5
Tomato puree 60 ml 1.02 4.1
Tomato paste 30 ml 2.29 9.1
Tomato sauce 227 ml 1.52 6.0
Spaghetti sauce 125 ml 2.44 9.7
Pizza sauce 60 ml 0.66 2.6
Chilli sauce 30 ml 0.30 1.2
Tomato ketchup 15 ml 0.53 2.1
Barbecue sauce 30 ml 0.06 0.2
Tomato juice 250 ml 2.20 8.7
Tomato soup 227 ml 0.79 3.1
Clam cocktail 250 ml 0.50 2.0
Bloody Mary mix 156 ml 0.15 0.6
Total 25.16
8 Factors affecting phytochemical
levels in tomatoes and tomato
products
8.1 Lycopene and other carotenoids
The levels of lycopene in tomatoes and tomato products vary considerably,
as seen in Table 4 (Section 3.2). There is variation between variety (which
may also be related to shapes, size and colour), degree of ripeness at
harvest, method of production, growing conditions, and extent of processing.
Unfortunately there are only a few studies relating particularly to New
Zealand varieties and growing conditions.
8.1.1 Cultivar
A number of researchers have shown that significant differences in lycopene
content occur between cultivars (Saini & Singh 1994; Hart & Scott 1995;
Chen et al. 2000; Molyneux 2001; Toor & Savage 2005; Kerkhofs 2003), the
latter three studies being New Zealand-based. Abushita et al. (2000) have
examined the variation in carotenoid levels in tomato cultivars grown on a
commercial scale (Table 14). As already discussed, since lycopene is related
to the redness of the tomato, some cultivars, such as the yellow cultivars and
Page 38

‘extended shelf life’ cultivars (with slow ripening characteristics, bred for the
fresh tomato market), contain minimal amounts of lycopene. It has also been
noted that cultivars with smaller fruits, such as the cherry tomatoes, appear to
have higher concentrations of antioxidants than larger tomatoes (Leonardi et
al. 2000; Raffo et al. 2002). Orlowski et al. (2001) noted that in addition to the
high lycopene levels in the three cherry-type cultivars they studied, vitamin C
content was also high. It has been hypothesised that this is due to the fact
that they possess a larger surface area to weight ratio, which is important as
lycopene reportedly concentrates in the pulp close to the skin of the fruit.
A wild relative of the domestic tomato, Lycopersicon pimpernellifolium,
produces tiny, currant-like fruit that are said to contain 40 times more
lycopene than regular tomatoes (Cox 2000) and is therefore a prime
candidate for use in the breeding of new hybrids. Researchers have also
isolated a crimson gene and found higher lycopene content in varieties
carrying this gene than in those without it (Thompson et al. 2000). A new,
conventionally bred tomato, Health Kick, is being advertised as possessing
“50% more lycopene compared to common tomato varieties”
(www.seminisgarden.com). A genetically modified cultivar, purportedly
containing twice the lycopene level of conventional culitivars, was reported by
Manzano (2001). Gomez et al. (2001) grew 15 different cultivars (standard
red type) under the same conditions and fruit harvested at optimum ripeness
had lycopene levels that varied from 5.04 to 13.46 mg/100 g FW.
Table 14: Carotenoid content of different tomato cultivars grown on a
commercial scale (adapted from Abushita et al. 2000).
Carotenoids (mg/100 g FW)
Cultivar Lutein
Lycopene
epoxide Lycopene cis-
Lycopene
β-
Carotene
Total
carotenoids
Amico 0.145 0.215 7.726 0.133 0.447 9.036
Casper 0.115 0.154 6.614 0.096 0.245 7.786
Gobe 0.143 0.116 5.918 0.127 0.402 7.150
Ispana 0.123 0.182 6.222 0.100 0.317 7.525
Pollux 0.348 0.148 5.140 0.097 0.210 6.799
?Soprano 0.429 0.361 8.646 0.107 0.321 11.026
Tenger 0.103 0.152 7.656 0.114 0.228 8.824
Uno 0.131 0.171 7.086 0.091 0.323 8.321
Zaphyre 0.303 0.173 6.950 0.113 0.375 8.907
Draco 0.076 0.208 6.868 0.090 0.291 8.191
Jovanna 0.138 0.282 11.606 0.082 0.339 13.205
K-541 0.118 0.256 9.954 0.092 0.283 11.248
Nivo 0.116 0.231 8.456 0.133 0.260 9.722
Simeone 0.361 0.200 9.879 0.103 0.296 11.882
Sixtina 0.332 0.249 10.510 0.111 0.318 12.521
Mean 0.199 0.207 7.949 0.106 0.310 9.476
Page 39

8.1.2 Growing conditions
Using lycopene content quantified in studies of field-grown tomatoes
(Abushita et al. 2000; Gomez et al. 2001;Takeola et al. 2001) and comparing
data with those from studies of greenhouse-grown tomatoes, Leonardi et al.
(2000) found tomatoes grown outdoors had a higher lycopene content than
those grown indoors. This may of course be related to different cultivars. An
old study found that β-carotene was lower in tomatoes grown under glass or
plastic than in the open field. Similarly, lycopene was lowest in tomatoes
grown under glass and highest in field-grown tomatoes (McCollum 1954). It is
difficult to know which parameters caused these results, but they may include
the level of intercepted light, and the high temperatures that occur under
protected growth conditions (Dumas et al. 2003). In some cases tomatoes
exposed to direct sunlight in the field may develop a poor colour because of
exposure to too high temperatures. Temperatures above 35°C stop lycopene
synthesis altogether, and temperatures below 12°C strongly inhibit this
process. However, in tomatoes harvested for processing, lycopene levels
have been shown to be enhanced by 5% at incubation temperatures of 30
and 34°C and by 33% at 37°C (Boothman et al. 1996). It has been postulated
that high temperatures inhibit the accumulation of lycopene because they
stimulate the conversion of lycopene to β-carotene. Best conditions appear to
be sufficiently high temperatures. However, outdoor-grown tomatoes require
good foliage cover to protect the fruit from direct exposure to the sun. It has
been shown that at favourable temperatures (22-25ºC) the rates of synthesis
of lycopene and β-carotene can be increased by illuminating tomato plants
during the ripening of the fruit (Dumas et al. 2003).
Arias et al. (2000) found that tomatoes ripened on the vine had one-third
higher lycopene than those ripened off the vine. In a study comparing
tomatoes grown in organic media with those grown in soil, Lacatus et al.
(1995) found lower dry matter and acidity, but increased sugar and lycopene
contents in the former. Looking at antioxidative activity in general, Leonardi et
al. (2000) found that plants under salt stress produced fruit with significantly
higher carotenoid levels than those irrigated with lower salinity water. It was
postulated that this was due to the concentration of the phloem sap, since
high salinity restricts water supply to the fruit via the phloem with the result
being a higher concentration of soluble solids and dry matter (including
carotenoids). Another study on tomatoes irrigated with water of varying
salinity showed an increase in lycopene levels only up to a certain point
(about 0.25%NaCl w/v) and a decrease after that (De Pascale et al. 2001).
One Japanese study found that in pink and red-type cultivars soil water deficit
increased the amount of lycopene per fresh weight in the outer pericarp
region of the tomato, and either increased or decreased vitamin C content
depending on the cultivar (Matsuzoe et al. 1998). However, another study
showed that fruit lycopene content decreased in response to moisture stress
(Naphade 1993). Further studies of the effects of water availability are
needed before firm conclusions can be drawn.
Mineral nutrition also has an impact on carotenoid levels. Highest fruit
lycopene levels have been achieved with lowest nitrogen (N) levels (Aziz
1968). N fertilisers have generally been thought to increase carotene
concentrations in plants but there are few data to confirm this. In one study
Page 40

tomatoes grown in pots did show an increase in fruit lycopene levels when
the N supply was increased (Montagu & Goh 1990). For tomatoes to develop
a good colour the N supply should be as low as possible without reducing the
fruit yield (Dumas et al. 2003). In contrast, increasing phosphorus levels in
tomatoes grown hydroponically (up to 100 mg/L) improved fruit colour and
lycopene content (Saito & Kano 1970). Various studies have looked at the
effect of potassium (K) on lycopene and other carotenoids and found it
produced more evenly coloured fruit and higher lycopene levels (Trudel &
Ozbun 1971; Winsor 1979). However, the levels used were very high and
could not be achieved with modern agricultural practices (Dumas et al. 2003).
In one study calcium was shown to significantly increase lycopene in
tomatoes grown in pots, from 8.5 to 34 mg/100 g FW (Subbiah & Perumal
1990). However, lycopene was lowered in another (Paiva et al. 1998),
although it has been suggested that this was due to a decrease in K
absorption.
Some growth and development regulators (e.g. CPTA and/or ethepon) have
also been shown to increase the carotenoid content of tomatoes (Dumas et
al. 2003).
8.1.3 Degree of ripeness and postharvest storage
Since the conversion of chlorophyll to lycopene is part of the ripening
process, it is not surprising that the highest levels of lycopene occur when the
fruit is at its reddest and ripest. It is also important that the degree of maturity
is determined if comparisons of lycopene content are made between
cultivars. The increase in lycopene content during ripening for one cultivar is
illustrated in Figure 11. It is interesting to note that lycopene content
continues to increase markedly during a period of storage at 18°C. Similar
patterns have been noted by other researchers with respect to other cultivars
(Hayman 1999; Molyneux 2000). Various patterns of carotenoid accumulation
have been reported. In a study in the open field, β-carotene increased
steadily during ripening whereas lycopene showed a sharp increase at the
‘breaker’ stage (Cabibel & Ferry 1980). The lycopene content is regarded as
a good index of maturation. In greenhouse-grown, vine-ripened tomatoes the
lycopene and β-carotene concentrations showed a gradual, linear increase
during the ripening process, whereas in postharvest-ripened fruit the
lycopene and β-carotene levels followed an exponential trend (Giovanelli et
al. 1999). The lycopene and β-carotene concentrations in postharvest-
ripened tomatoes (12.5-13.0 and 1.2 mg/100 g FW respectively) were nearly
twice as high as the vine-ripened tomatoes (7.5-8.0 and 0.5-0.7 mg/100 g FW
respectively) that had the same colour index. Appropriate postharvest
storage conditions can, therefore, increase the lycopene content of tomatoes
(Dumas et al. 2003). Fruit bruising at the breaker stage can decrease
carotenoids in the ripe fruit (Moretti et al. 1998).
Page 41

Figure 6: Changes in carotenoid levels during tomato fruit ripening (from
www.britishtomatoes.co.uk). Stage of ripeness: 1 = first signs of colour
change, sometimes referred to as "breaker" stage; 5 = half-ripe or
orange; 9 = red; 9 + 7 days = colour stage 9 plus 7 days storage at room
temperature (18°C).
8.1.4 Effects of cooking/processing
In the course of production, the availability of some nutrients may be
enhanced, whilst quantities of others, such as the heat labile vitamin C, are
lost. A number of factors affect the nutritional value of tomatoes, including
storage conditions, method of processing, moisture, temperature and the
presence of oxidants and lipids. Macrae et al. (1993) found that maximum
ripening and colour development for tomatoes in storage occurred at
between 20 and 24°C, with poor ripening at temperatures lower than 13°C.
The food matrix (i.e. the lipid and protein constituents of chromoplasts as well
as the fibre contained within the tomato fruit) may contribute greatly to the
stability of the all-trans form of lycopene in the fruit. This is supported by the
observation that when tomatoes are heat processed only minor isomerisation
is noted. Heat treatment improves the bioavailability of lycopene without
significantly changing the cis-isomer composition of the heat-treated foods
(Stahl & Sies 1992; Gärtner et al. 1997). Various types of dietary fibre have
been shown to reduce the carotenoid bioavailability of some foods (Erdman
et al. 1986).
The processing of tomatoes usually involves heat treatment and/or
homogenisation. Tables 4 and 5 (see Section 3.2) and 15 give examples of
lycopene concentration in some processed tomato products. These results
reflect several different factors involved during processing.
Page 42

Table 15: Change in the carotenoid content (mg/100 g DM) of tomato as a function of processing
(adapted from Abushita et al. 2000).
Variety Lutein
Lycopene
epoxide
all-trans-
Lycopene Cis-
Lycopene
all-trans-β-
Carotene cis-
lycopene
Total
carotenoids
Raw
material
1.98 4.14 119.8 2.06 3.72 <0.10 143.0
Hot-break
extract
1.85 3.70 122.0 2.55 3.85 0.39 131.9
Tomato
paste
1.92 4.73 162.8 2.52 2.63 0.97 184.9
As already discussed in Section 6.1, processing appears to make lycopene
more bioavailable (Stahl & Sies 1992; Gärtner et al. 1997). The health
benefits resulting from isomerisation, however, are balanced to some extent
by loss due to the same treatment that caused it. Table 24 gives the amount
of lycopene lost from tomato juice over various temperatures and various
heating times. It is evident that both temperature and the length of heating
affect the extent of lycopene breakdown. It has also been reported that
serious losses of lycopene can occur when the holding times at high
temperatures are long (Shi & Le Maguer 2000). This process, however, was
not observed by Nguyen & Schwarz (1999) who suggested that lycopene
was relatively resistant to degradation, including by isomerisation, and
Thompson et al. (2000) who found little difference in lycopene content
between uncooked and samples cooked at 100°C, for 4, 8 and 16 minutes.
Similarly Abushita et al. (2000) observed no change in lycopene
concentration as fresh tomatoes were processed into paste.
Table 16: Loss rate in tomato juice during heating (from Shi & Le Maguer
2000).
Lycopene loss (%)
Heating
temperature (°C)
Heating time
1 min
Heating time
3 min
Heating time
7 min
90 0.6 0.9 1.1
100 0.9 1.4 1.7
110 2.2 3.2 4.4
115 2.7 4.5 7.0
118 3.7 6.0 9.1
121 4.6 7.3 10.6
124 5.5 8.5 12.5
127 6.5 9.9 14.6
130 7.4 11.5 17.1
Page 43

Shi & Le Maguer (2000) found that thermal processing in the forms of
bleaching, retorting and freezing generally caused a loss of lycopene, due
mainly to isomerisation and oxidation. However, once processed, frozen and
heat sterilised foods exhibited excellent lycopene stability for the term of their
normal shelf life. Takeoka et al. (2001) noted that the initial Brix level of the
raw tomatoes appeared to influence the amount of lycopene that was lost
during the processing of tomatoes into paste, but hypothesised that this could
also have been the result of longer processing in order to obtain the desired
Brix level. This study also found that overall antioxidant activity was greater
with tomato paste than fresh tomatoes, but also found that in addition to the
antioxidative effect of the lycopene present, there appeared to be significant
antioxidant activity due to the polyphenols in the tomato.
There are varying reports on the presence of cis-isomers of lycopene.
Nguyen & Schwartz (1998) showed only minor changes in their levels during
a range of thermal treatments (Table 17). However, Schierle et al. (1996) did
show some significant levels of cis-isomers in a range of tomato products
(Table 18). The presence of other components or influence of factors may
explain these effects rather than any thermal processing. Heat, light, acids
and other factors have been reported to cause isomerisation (Schierle et al.
1996; Nguyen & Schwartz 1998; Shi et al. 1999). Swartz et al. (1999) have
further investigated effects of thermal processing on isomerisation of
lycopene and other tomato carotenoids. Upon thermal treatment β-carotene
and lutein isomerise to a greater extent than δ-carotene, γ-carotene and
lycopene. The presence of lipid was found not to influence the extent or
likelihood of lycopene and other tomato carotenoids in the all-trans
configuration to isomerise. Likewise the presence of different carotenoids did
not influence the formation of lycopene cis-isomers.
Table 17: Lycopene isomers in various thermally processed tomato
products (from Nguyen & Schwartz 1998).
Sample
Total lycopene
(mg/100 g DW) Cis-isomers (%)
Peeled tomato 149.89 5.37
Tomato juice (hot-break) 161.23 5.89
Tomato juice (retorted) 180.10 3.56
Tomato (whole, retorted) 183.49 3.67
Tomato paste
(concentrated)
174.79 5.07
Tomato paste (retorted) 189.26 4.07
Tomato soup (retorted) 136.76 4.34
Tomato sauce (retorted) 73.33 5.13
Page 44

Table 18: Lycopene isomers in commercial tomato products (data
Schierle et al. 1996).
Sample
Total lycopene
(mg/100 g FW)
All-trans
(%)
5-cis
(%)
9-cis
(%)
13-cis
(%)
Other cis
(%)
Tomato paste
(Tomatenmark, Panocchia, Italy)
52 96 4 <1 <1 <1
Tomato paste
(Maracoli, Kraft, Germany
3.7 91 5 1 2 <1
Tomato ketchup
(Hot Ketchup, Del Monte, Italy)
9.5 88 7 2 3 1
Tomato ketchup
(Hot Ketchup, Heinz, USA)
3.0 77 11 5 7 1
Instant meal
(Eier-Ravioli, Hero, Switzerland)
0.6 76 8 5 6 5
Sauce
(Hamberger Relish, Heinz, The
Netherlands)
3.0 93 5 <1 3 <1
Sauce
(Sauce Bolognaise, Barilla, Italy)
9.2 67 14 14 5 8
Canned tomatoes
(Chris, Roger Sud, Italy)
7.1 84 5 5 5 3
Dewanto et al. (2002) showed that thermal processing elevated total
antioxidant activity and bioaccessible lycopene content in tomatoes and
produced no significant changes in the total phenolics and total flavonoid
content, although loss of vitamin was observed (Table 19).
Table 19: Percent changes in selected antioxidants and antioxidant
activity in processed tomatoes compared to unprocessed fruit (from
Dewanto et al. 2002).
Processing time at 88°C
2 min 15 min 30 min
Vitamin C -10.2 -15.5 -29.4
Lycopene 54.4 171.1 164.3
Total antioxidant activity 28.1 33.9 62.2
Page 45

8.2 Phenolics
8.2.1 Raw tomatoes
Factors affecting the levels of phenolics in vegetables have been studied by
numerous researchers. Mineral nutrition can have a major influence on
phenolic accumulation, and a limited nitrogen supply is typically associated
with higher levels of phenolics in the plant (Parr & Bolwell 2000). Other
environmental factors that can influence phenolic metabolism include
ambient temperature. Lower temperature increases some phenolics, in
particular the anthocyanins (although these are not present in tomatoes).
Although many stresses tend to increase the levels of phenolics, water deficit
usually tends to impair accumulation. One of the major environmental
controls on phenolic production is light, where both photoperiod and light
intensity can have an effect.
There have been limited studies specifically looking at tomatoes and the
factors affecting the levels of phenolics in the fruit. Various researchers have
noted significant differences in phenolic levels between cultivars (Stewart at
al. 2000; Martinez-Valverde et al. 2002). However, Senter et al. (1988) found
that the levels did not vary significantly in the three cultivars they tested.
Interestingly Minoggio et al. (2003) found that almost all the tomato lines they
tested with low carotenoid content produced high levels of phenolics, and
consequently had the strongest antioxidant activity.
The most comprehensive study of factors affecting levels of phenolics in
tomato was conducted by Stewart at al. (2000). Their main findings were:
 fruit size: greater skin/volume ratio enhances flavonol content,
 country of origin: tomatoes from Spain and South Africa contained higher
levels of flavonols than UK fruits. Spanish tomatoes are usually field-
grown whereas those from the UK are usually glasshouse-grown and
therefore exposed to lower UV levels,
 effect of season: there was some fluctuation, but not dramatic. However,
it was only examined in Spain,
 effect of cultivar: significant differences were observed even when
cultivars were grown under same conditions.
In another study with cherry tomatoes, plants grown in greenhouses with high
light had approximately a twofold higher content of soluble phenolics than
plants grown in low light (Wilkens et al. 1996). In all parts of the tomato the
phenolics tend to increase from the green stage to the mid-ripe stage before
decreasing to original levels at the ripe stage (Senter et al. 1988). In other
cultivars the highest quantities of phenolic acids were present in the pulp at
the earliest stages of development and decreased during ripening (Buta &
Spaulding 1997). A similar pattern was observed for rutin in the skin.
Variations in phenolic content during vine and postharvest ripening were also
investigated by Giovanelli et al. (1999). The total phenolic content was higher
in postharvest-ripened fruit than in vine-ripened fruit.
Attempts have been made to increase the antioxidant level of tomatoes by
modifying the flavonoid biosynthetic pathway (Bovy et al. 2002; Verhoeyen et
Page 46

al. 2002). In one case up to a 78-fold increase in total fruit flavonols was
achieved (Verhoeyen et al. 2002). It was also possible to produce flavonoids
in the tomato fruit flesh, a tissue that normally produces little or no flavonoids
(Bovy et al. 2002).
8.2.2 Processing/cooking
There appears to have been little study of the effects of processing on the
phenolic content of tomatoes. The flavonol content of some processed
tomato products is shown in Table 20. In contrast to tomato fruit, which
contain almost exclusively conjugated quercetin, up to 30% of the quercetin
in processed products is in the free form (Stewart et al. 2000). Hydrolysis of
flavonol conjugates during cooking of tomatoes was not noted in an earlier
study by this research group (Crozier et al. 1997). Thus, it was hypothesised
that the accumulation of free quercetin in juices, puree and paste may have
been a consequence of enzymatic hydrolysis of rutin and other quercetin
conjugates during pasteurisation and processing procedures. The
concentration of flavonols in some tomato products is likely to depend on the
extraction of flavonols from the skin during initial processing, which often
involves heating. Low levels of flavonols in canned compared to fresh fruit
could be due to boiling, as cooking in this manner results in up to an 80%
loss of flavonols (Crozier et al. 1997), presumably by leaching from the skins.
One study was found reporting that, of the flavonoids, naringenin was the
main one affected (a reduction in concentration) during processing of
tomatoes into sauce (Re et al. 2002).
Table 20: The flavonol content (mg/100 g FW or for juice and soup mg/100 ml) of selected tomato-based food
products (adapted from Stewart et al. 2000).
Tomato
product Brand
Free
quercetin
Free
kaempferol
Conjugated
quercetin
Conjugated
kaempferol
Total
flavonol
Free
flavonol %
Fresh
tomatoesa
- 0.01 0.02 0.77 0.05 0.85 3.4
Tomato
soup
Safeway 0.03 Nd 0.12 nd 0.15 19.6
Tomato
juice
Del Monte 0.29 0.04 1.15 0.04 1.52 21.6
Libby’s 0.35 0.04 1.27 0.03 1.69 22.9
Canned
cherry
tomatoes
Napolina Nd Nd 0.17 0.01 0.18 0
Canned
plum
tomatoes
Napolina Nd Nd 0.03 nd 0.04 0
Pasta
sauce
Dolmio 0.12 Nd 0.79 0.01 0.92 12.6
Ketchup Heinz 0.04 Nd 0.82 0.01 0.88 4.5
Puree Casinop 0.38 0.06 3.25 0.02 3.71 11.9
Masque
D’or
0.54 Nd 1.09 0.03 1.66 32.5
Safeway 0.95 Nd 6.14 0.13 7.22 13.2
a Average of a number of cultivars.
Page 47

8.3 Vitamins
Changes in antioxidant vitamins are probably less important than carotenoids
or phenolics. Vitamin E is only present in very low amounts and there is little
information on factors affecting its level in tomatoes. Variations in the vitamin
E content amounting to about one to threefold (from 0.1 to 0.32 mg/100 g FW
for α-tocopherol and from 0.12 to 0.40 mg/100 g FW for total tocopherols)
have been observed in various Hungarian cultivars (Abushita et al. 1997).
Vitamin C is present in reasonable levels in the raw fruit but it is significantly
affected by processing and so is comparatively low in processed products.
Some authors have stated that the variations in vitamin C content due to
cultivar are fairly small in comparison with those resulting from growth
conditions (Hamner et al. 1945). However, there are large variations within
tomato species (from 8 up to 119 mg/100 g FW in some wild species)
(Stevens & Rick 1986). Attempts to increase the vitamin C content of the
cultivated tomato through traditional breeding have had little success.
Variations ranging from 25 to 48 mg/100 g FW were observed for various
cultivars of tomato grown in Hungary (Abushita et al. 1997).
Fruit ripening at relatively high temperatures, whether on or off the plant,
along with relatively low light intensity levels probably leads to a decrease in
the ascorbic acid content due to oxidation (Murneek et al. 1954). Under
greenhouse conditions seasonal variations in the vitamin C content ranged
from 7 to 23 mg/100 g FW at the mature-green stage and were directly
correlated with temperature variations (Liptay et al. 1986). Light intensity prior
to harvesting can also affect ascorbic acid content. Transfer of fruit from
shade to sun results in increases in ascorbic acid content (Hamner et al.
1945). Greenhouse-grown tomatoes were usually found to have lower
vitamin C levels than those grown outdoors, chiefly due to the lower light
intensity and shorter day length (Murneek et al. 1954). A seasonal increase
has been observed in the ascorbic acid content of field-grown fruit from early
to late summer (Dumas et al. 2003).
Water shortage seems generally to increase the vitamin C content of the fruit,
as well as the dry matter and soluble solid content (Dumas et al. 2003).
Supplementary nitrogen, especially at high rates, tends to decrease the
tomato vitamin C content, possibly due to the increased shading caused by
the greater development of plant foliage (Dumas et al. 2003). Increasing
phosphorus concentrations in hydroponics did not significantly affect vitamin
C content (Saito & Kano 1970). As with lycopene, calcium application to
tomatoes grown in pots resulted in a significant increase in vitamin C
(Subbiah & Perumal 1990). It has been reported in several papers that the
vitamin C content of tomatoes could increase with the supply of combined
fertilisers (Dumas et al. 2003). Some plant growth regulators (e.g. alar,
gibberelic acid, cycocel and phosphon) have also been shown to increase the
vitamin C content of tomatoes (Dumas et al. 2003).
A French study showed that vitamin C was higher in tomatoes grown by
conventional methods than those produced organically (Auclair et al. 1995).
The vitamin C content of tomatoes picked green and allowed to ripen at 22-
24.5°C increased from 11 to 26 mg/100 g FW (Murneek et al. 1954). Similar
patterns have been observed in other studies (Venter 1977; Shi et al. 1999),
Page 48

but Abushita et al. (1997) reported an increase during initial reddening but
then a decrease. The vitamin C content of fruit bruised at the breaker stage
decreased at the ripe stage compared to undamaged fruit (Moretti et al.
1998). Variations in vitamin C content during vine and postharvest ripening
were also investigated by Giovanelli et al. (1999). In postharvest-ripened fruit,
ascorbic acid decreased and then returned to original levels, while in vine-
ripened fruit it increased and then decreased to a similar or slightly lower
level.
There are limited specific data on the loss of vitamin C in tomatoes during
processing. One study by Abushita et al. (2000) did show loss of activity
(Table 21). Dewanto et al. (2002) also showed that thermal processing
resulted in a loss of vitamin C (Table 18).
Table 21: Change in ascorbic acid
content of tomato as a function of
processing (adapted from Abushita et al.
2000).
Processing steps
Ascorbic acid
(mg/g dm)
Raw material 3.17
Hot-break extract 1.96
Tomato paste 1.45
Loss % 54.6%
8.4 Summary
Many of the studies of lycopene content in tomatoes and tomato products
were carried out some time ago and many did not use commercially relevant
cultivars. All experimental details are often not reported, which makes it
difficult to compare results and may explain some of the contradictory
findings. Some give different results for different antioxidants. For example,
water storage during cropping may increase vitamin C level but reduce
lycopene content. Direct sunlight may enhance accumulation of phenolics
and vitamin C but foliage cover may help lycopene accumulation. Further
research is required with commercially relevant processing cultivars to
establish protocols for enhancing phytochemical content in tomatoes.
9 Promoting nutritional attributes
Dietary intakes of tomatoes and tomato products may be associated with
decreased risk of various diseases, including cancers, especially prostate,
and heart disease. The benefits have been attributed to the lycopene
content, but it is probable other phytochemicals in tomatoes also contribute to
these benefits. Lycopene is the main carotenoid present in tomatoes and
Page 49

unlike β-carotene, has no provitamin A activity. However, it is a powerful
antioxidant and other modes of action may also be responsible for its health
benefits (e.g. modulation of intercellular gap junction communication,
hormonal and immune systems and metabolic pathways). In addition to
lycopene, and other carotenoids (e.g. β-carotene, phytoene, phytofluene),
tomatoes contain a range of other phytochemicals with potential health
benefits, including phenolic acids (e.g. coumaric and chlorogenic acids),
flavonoids (e.g. quercetin-3-rutinoside, naringenin) and antioxidant vitamins
(vitamins C and E). Lycopene is readily absorbed from different food
sources, distributes to different tissues in the human body and has been
demonstrated to have antioxidant properties within the body. Serum levels of
lycopene have been related to a reduced risk of several types of cancer.
However, more research is still required to fully understand the health
benefits of tomatoes/lycopene, the interactions between the phytochemicals
in tomatoes, and establish clear dietary guidelines.
The more intense red the tomato is, the more lycopene it is likely to contain.
Locally grown fruit, especially some of the more niche tomatoes (e.g. vine)
appear to brighter in colour than the paler imported Australian varieties.
Similarly, smaller tomatoes tend to have a higher lycopene content than
larger cultivars. Storage can also affect lycopene levels and appropriate
cooking methods appear to enhance the absorption of lycopene by the body.
Consuming the whole fruit, including the skins and seeds maximises the
delivery of the potential health benefits of the tomato.
10 References
Abushita, A.A.; Daood, H.G.; Biacs, P.A. 2000: Change in carotenoids and
antioxidant vitamins in tomato as a function of varietal and technological
factors. Journal of Agricultural and Food Chemistry 48(6): 2075-2081.
Abushita, A.A.; Hebshi, E.A.; Daood, H.G.; Biacs, P.A. 1997: Determination
of antioxidant vitamins in tomatoes. Food Chemistry 60(2): 207-212.
Agarwal, S.; Rao, A.V. 1998: Tomato lycopene and low density lipoprotein
oxidation: a human dietary intervention study. Lipids 33: 981-984.
Andreassi, M.; Stanghellini, E.; Ettorre, A.; Di Stefano, A.; Andreassi, L. 2004:
Antioxidant activity of topically applied lycopene. Journal of the European
Academy of Dermatology and Venereology 18: 52-55
Arias, R.; Lee, T.C.; Logendra, L; James, H. 2000: Correlation of lycopene
measured by HPLC with the L*, a*, b* colour readings of a hydroponic tomato
and the relationship of maturity with colour and lycopene content. Journal of
Agricultural and Food Chemistry 48: 1697-1702.
Athar, N.; Spriggs, T.W.; Taptiklis, E.L.; Taylor, G.J. 2001: The concise New
Zealand food composition tables. 5th Edition. Christchurch, New Zealand
Institute for Crop & Food Research Limited/Ministry of Health.
Auclair, L.; Zee, J.A.; Karam, A.; Rochat, E. 1995: Valeur nutritive, qualité
organoleptique et produtivité des tomates de serre en fonction de leur mode
Page 50

de production: biologique, conventionnel, hydroponique. Sciences des
Aliments 15: 511-528.
Aziz, A.B.A. 1968: Seasonal changes in the physical and chemical
composition of tomato fruits as affected by nitrogen levels. Meded
Landbouwhogescholl Wageningen: 68-77. [cited in Dumas et al. 2003]
Barbagallo, C.; Cavera, G.; Sapienza, M; Noto, D.; Cefalu, A.; Polizzi, D.;
Onorato, F.; Rini, G.; Di Fede, G.; Pagano, M.; Montalto, G.; Rizzo, M.;
Descovich, G.; Notarbartolo, A.; Averna, M. 2002: Nutritional characteristics
of a rural Southern Italy population: the Ventimiglia di Sicilia project. Journal
of the American College of Nutrition 21: 523-529.
Batieha, A.M.; Armenian, H.K.; Norkus, E.P.; Morris, J.S.; Spate, V.E.;
Comstock, G.W. 1993: Serum micronutrients and the subsequent risk of
cervical cancer in a population-based nested case-control study. Cancer
Epidemiology Biomarkers & Prevention 2(4): 335-339.
Beecher, G.R. 1998: Nutrient content of tomatoes and tomato products.
Proceedings of the Society for Experimental Biology and Medicine 218(2):
98-100.
Benito, E.; Obrador, A.; Stiggelbout, A.; Bosch, F.X.; Mulet, M.; Munoz, N.;
Kaldor, J. 1990: A population-based case-control study of colorectal cancer in
Majorca. I. Dietary factors. International Journal of Cancer 45(1): 69-76.
Bierman, F.Z. 1991: Guidelines for diagnosis and management of cardiac
disease in children with HIV infection. Journal of Pediatrics 119(1(Pt 2)): S53-
6.
Bjelke, E. 1974: Epidemiologic studies of cancer of the stomach, colon, and
rectum; with special emphasis on the role of diet. Scandanavian Journal of
Gastroenterololgy 31(Suppl.): 1-235.
Block, G.; Patterson, B.; Subar, A. 1992: Fruit, vegetables, and cancer
prevention: a review of the epidemiological evidence. Nutrition and Cancer
18(1): 1-29.
Bohm, V.; Bitsch, R. 1999: Intestinal absorption of lycopene from different
matrices and interaction with other carotenoids, the lipid status and the
antioxidant capacity of human plasma. European Journal of Nutrition 38: 118-
125.
Bohm, F.; Tinkler, J.H.; Truscott, T.G. 1995: Carotenoids protect against cell
membrane damage by the nitrogen dioxide radical. Nature Medicine 1(2): 98-
99.
Boileau, A.C.; Merchen, R.N.; Wasson, K.; Atkinson, C.A.; Erdman, J.W.
1999: Cis lycopene is more bioavailable than trans lycopene in vitro and in
vivo in lymph-cannulated ferrets. Journal of Nutrition 129: 1176-1181.
Boothman, S.; Britton, G.; Collin, H.A.; Giadevoni, P. 1996: Effects of
temperature on lycopene accumulation in tomato. Journal of Experimental
Botany 47 (Suppl.): Annual Meeting of the Society for Experimental Biology,
Plant Biology Abstracts, Lancaster.
Bovy, A.; de Vos, R.; Kemper, M.; Schijlen, E.; Pertejo, M.A.; Muir, S.;
Collins, G.; Robinson, S.; Verhoeyen, M.; Hughes, S.; Santos-Buelga, C.; van
Page 51

Tunen, A. 2002: High-flavonol tomatoes resulting from the heterologous
expression of the maize transcription factor genes LC and C1. Plant Cell
14(10): 2509-2526.
Brady, W.E.; Mares-Perlman, J.A.; Bowen, P.; Stacewicz-Sapuntzakis, M.
1996: Human serum carotenoid concentrations are related to physiologic and
lifestyle factors. Journal of Nutrition 126(1): 129-137.
Bramley, P.M. 2000: Is lycopene beneficial to health? Phytochemistry
54:223-236.
British Tomato Growers Association www.britishtomatoes.co.uk. Accessed
06/05/2003
Brune, M.; Hallberg, L.; Skanberg, A.B. 1991: Determination of iron-binding
phenolic groups in foods. Journal of Food Science 56: 128.
Bugianesi, R.; Catasta, G.; Spigno, P.; D’Uva, A.; Maiani, G. 2002:
Naringenin from cooked tomato paste is bioavailable in men. Journal of
Nutrition 132(11): 3349-3352.
Buiatti, E.; Palli, D.; Decarli, A.; Amadori, D.; Avellini, C.; Bianchi, S.; Biserni,
R.; Cipriani, F.; Cocco, P.; Giacosa, A. 1989: A case-control study of gastric
cancer and diet in Italy. International Journal of Cancer 44(4): 611-616.
Buta, J.G.; Spaulding, D.W. 1997: Endogenous levels of phenolics in tomato
fruit during growth and maturation. Journal of Plant Growth Regulation 16:
43-46.
Cabibel, M.; Ferry, P. 1980: Evolution de la teneur en carotenoids de la
tomate en fonction de la maturation et des conditions culturales. Annales de
Technologie Agricole 29(1): 27-46. [cited in Dumas et al. 2003]
Campbell, D.R.; Gross, M.D.; Martini, M.C.; Grandits, G.A.; Slavin, J.L.;
Potter, J.D. 1994: Plasma carotenoids as biomarkers of vegetable and fruit
intake. Cancer Epidemiology Biomarkers & Prevention 3(6): 493-500.
Castenmiller, J.J.M.; West, C.E. 1998: Bioavailability and bioconversion of
carotenoids. Annual Review of Nutrition 18: 19-38.
Cesarini, J.P.; Michel, L.; Maurette, J.M.; Adhoute, H.; Bejot, M. 2003:
Immediate effects of UV radiation on the skin: modification by an antioxidant
complex containing carotenoids. Photodermatol Photoimmunol Photomed 19:
182-189.
Chen, Y.; Wu, J.J.; Tsai, M.J.; Liu, M.S. 2000: Effects of storage and thermal
treatment on the antioxidant activity of tomato fruits. Taiwanese Journal of
Agricultural Chemistry and Food Science 38(4): 353-360.
Chuang, C.Z.; Subramaniam, P.N.; LeGardeur, B.Y.; Lopez, A. 1998: Risk
factors for coronary artery disease and levels of lipoprotein (a) and fat soluble
antioxidant vitamins in Asian Indians of USA. Indian Heart Journal 50: 285-
291.
Clinton, S.K. 1998: Lycopene: chemistry, biology, and implications for human
health and disease. Nutrition Reviews 56: 35-51.
Clinton, S.K.; Emenhiser, C.; Schwartz, S.J.; Bostwick, D.G.; Williams, A.W.;
Moore, B.J.; Erdman, J.W. Jr. 1996: cis-trans lycopene isomers, carotenoids,
Page 52

and retinol in the human prostate. Cancer Epidemiology Biomarkers &
Prevention 5(10): 823-833.
Cody, V.; Middleton, E. Jr.; Harborne, J.B. 1986: Plant flavonoids in biology
and medicine: biochemical, pharmacological, and structure-activity
relationships. New York, Alan Liss, Inc.
Coodley, G.O.; Coodley M.K.; Nelson, H.D. 1995: Micronutrients in HIV-
infected women. Journal of Womens Health 4: 303-311.
Cook-Mozaffari, P.J.; Azordegan, F.; Day, N.E.; Ressicaud, A.; Sabai, C.;
Aramesh, B. 1979: Oesophageal cancer studies in the Caspian Littoral of
Iran: results of a case-control study. British Journal of Cancer 39(3): 293-309.
Correa, P.; Fontham, E.; Pickle, L.W.; Chen, V.; Lin, Y.P.; Haenszel, W.
1985: Dietary determinants of gastric cancer in south Louisiana inhabitants.
Journal of the National Cancer Institute 75(4): 645-654.
Cox, S. 2000: http://lamar.colorstate.edu/~samcox/Tomato.html
Cramer, D.W.; Harlow, B.L.; Kuper, H.; Titus-Ernstoff, L. 2001: Carotenoids,
antioxidants and ovarian cancer risk in pre- and postmenopausal women.
International Journal of Cancer 94(1): 128-134.
Crozier, A.; Lean, M.E.J.; McDonald, M.S.; Black, C. 1997: Quantitative
analysis of the flavonoid content of commercial tomatoes, onions, lettuce,
and celery. Journal of Agricultural and Food Chemistry 45(3): 590-595.
Darby, S.; Whitley, E.; Doll, R.; Key, T.; Silcocks, P. 2001: Diet, smoking and
lung cancer: a case-control study of 1000 cases and 1500 controls in South-
West England. British Journal of Cancer 84(5): 728-735.
Davies, J.N.; Hobson, G.E. 1981: The constituents of tomato fruit - the
influence of environment, nutrition, and genotype. CRC Critical Reviews in
Food Science and Nutrition 15(3): 205-280.
De Pascale, S.; Maggio, A.; Fogliano, V.; Ambrosino, P.; Ritieni, A. 2001:
Irrigation with saline water improves carotenoids content and antioxidant
activity of tomato. Journal of Horticultural Science & Biotechnology 76(4):
447-453.
De Stefani, E.; Oreggia, F.; Boffetta, P.; Deneo-Pellegrini, H.; Ronco, A.;
Mendilaharsu, M. 2000: Tomatoes, tomato-rich foods, lycopene and cancer
of the upper aerodigestive tract: a case-control in Uruguay. Oral Oncology
36(1): 47-53.
Dewanto, V.; Wu, X.; Adom, K.K.; Liu, R.H. 2002: Thermal processing
enhances the nutritional value of tomatoes by increasing total antioxidant
activity. Journal of Agricultural and Food Chemistry 50: 3010-3014.
Di Mascio, P.; Kaiser, S.; Sies, H. 1989: Lycopene as the most efficient
biological carotenoid singlet oxygen quencher. Archives of Biochemistry and
Biophysics 274: 532-538.
Dorgan, J.F.; Sowell, A.; Swanson, C.A.; Potischman, N.; Miller, R.;
Schussler, N.; Stephenson, H.E. Jr. 1998: Relationships of serum
carotenoids, retinol, alpha-tocopherol, and selenium with breast cancer risk:
results from a prospective study in Columbia, Missouri (United States).
Cancer Causes & Control 9: 89-97.
Page 53

Dumas, Y.; Dadomo, M.; Di Lucca, G.; Grolier, P. 2003: Effects of
environmental factors and agricultural techniques on antioxidant content of
tomatoes. Journal of the Science of Food and Agriculture 83(5): 369-382.
Dutta-Roy, A.K.; Crosbie, L.; Gordon, M.J. 2001: Effects of tomato extract
onhuman platelet aggregation in vitro. Platelets 12: 218-227.
Elinder, L.S.; Hadell, K.; Johansson, J.; Molgaard, J.; Holme, I.; Olsson, A.G.;
Walldius, G. 1995: Probucol treatment decreases serum concentrations of
diet-derived antioxidants. Arteriosclerosis Thrombosis and Vascular Biology
15: 1057-1063.
Erdman, J.W. Jr.; Fahey, G.C. Jr.; White, C.B. 1986: Effects of purified
dietary fiber sources on beta-carotene utilization by the chick. Journal of
Nutrition 116(12): 2415-2423.
Erlund, I.; Alfthan, G.; Maenpaa, J.; Aro, A. 2001: Tea and coronary heart
disease: the flavonoid quercetin is more bioavailable from rutin in women
than in men. Archives of Internal Medicine 161(15): 1919-1920.
Erlund, I.; Kosonen, T.; Alfthan, G.; Maenpaa, J.; Perttunen, K.; Kenraali, J.;
Parantainen, J.; Aro, A. 2000: Pharmacokinetics of quercetin from quercetin
aglycone and rutin in healthy volunteers. European Journal of Clinical
Pharmacology 56(8): 545-553.
Flood, V.; Smith, W.; Wang, J.J.; Manzi, F.; Webb, K.; Mitchell, P. 2002:
Dietary antioxidant intake and incidence of early age-related maculopathy:
the Blue Mountains Eye Study. Ophthalmology 109(12): 2272-2278.
Ford, E.S.; Will, J.C.; Bowman, B.A.; Narayan, K.M. 1999: Diabetes mellitus
and serum carotenoids findings from the Third National and Nutrition
Examination Survey. American Journal of Epidemiology 149: 168-176.
Forman, M.R.; Beecher, G.R.; Lanza, E.; Reichman, M.E.; Graubard, B.I.;
Campbell, W.S.; Marr, T.; Yong, L.C.; Judd, J.T.; Taylor, P.R. 1995: Effect of
alcohol consumption on plasma carotenoid concentrations in premenopausal
women: a controlled dietary study. American Journal of Clinical Nutrition
62(1): 131-135.
Forman, M.R.; Johnson, E.J.; Lanza, E.; Graubard, B.I.; Beecher, G.R.;
Muesing, R. 1998: Distribution of individual carotenoids in lipoproteins of
premenopausal women: A controlled dietary study. American Journal of
Clinical Nutrition 67: 81-87.
Forman, M.R.; Lanza, E.; Yong, L.C.; Holden, J.M.; Graubard, B.I.; Beecher,
G.R.; Meltiz, M.; Brown, E.D.; Smith, J.C. 1993: The correlation between two
dietary assessments of carotenoid intake and plasma carotenoid
concentrations: application of a carotenoid food-composition database.
American Journal of Clinical Nutrition 58(4): 519-524.
Franceshi, S.; Bidoli, B.; Laveochia, C.; Talamini, R.; D'Avanzo, B.; Negri, E.
1994: Tomatoes and risk of digestive tract cancers. International Journal of
Cancer 59: 181-184.
Frankel, E.N.; Kanner, J.; German, J.B.; Parks, E.; Kinsella, J.E. 1993:
Inhibition of oxidation of low-density lipoprotein by phenolic substances in red
wine. Lancet 341: 454-456.
Page 54

Freeman, V.L.; Meydani, M.; Yong, S.; Pyle, J.; Wan, Y.; Arvizu-Durazo, R.
2000: Prostatic levels of tocopherols, carotenoids, and retinol in relation to
plasma levels and self-reported usual dietary intake. American Journal of
Epidemiology 151: 109-118.
Fuhramn, B.; Elis, A.; Aviram, M. 1997: Hypocholesterolemic effect of
lycopene and β-carotene is related to suppression of cholesterol synthesis
and augmentation of LDL receptor activity in macrophage. Biochemical and
Biophysical Research Communications 233: 658-662.
Gann, P.H.; Ma, J.; Giovannucci, E.; Willett, W.; Sachs, F.M.; Hennekens,
C.H.; Stammpfer, M.J. 1999: Lower prostate cancer risk in men with elevated
plasma lycopene levels: results of a prospective analysis. Cancer Research
59:1225-1230. [cited in Giovannucci 1995]
Garland, M.; Willett, W.C.; Manson, J.E.; Hunter, D.J. 1993: Antioxidant
micronutrients and breast cancer. Journal of the American College of
Nutrition 12(4): 400-411.
Gärtner, C.; Stahl, W.; Sies, H. 1997: Lycopene is more bioavailable from
tomato paste than from fresh tomatoes. American Journal of Clinical Nutrition
66: 116-122.
Gaziano, J.M.; Johnson, E.J.; Russell, R.M.; Manson, J.E.; Stampfer, M.J.;
Ridker, P.M.; Frei, B.; Hennekens, C.H.; Krinsky, N.I. 1995: Discrimination in
absorption or transport of beta-carotene isomers after oral supplementation
with either all-trans- or 9-cis-beta-carotene. American Journal of Clinical
Nutrition 61(6): 1248-1252.
Giovanelli, U.; Lavelli, V.; Pen, C.; Nobili, S. (1999). Variation in antioxidant
components of tomato during vine and post-harvest ripening. Journal of the
Science of Food and Agriculture 79: 1583-1588.
Giovannucci, E. 1999: Tomatoes, tomato-based products, lycopene, and
cancer: review of the epidemiologic literature. Journal of the National Cancer
Institute 91: 317-331.
Giovannucci, E. 2002: A review of epidemiologic studies of tomatoes,
lycopene, and prostate cancer. Experimental Biology and Medicine
(Maywood) 227(10): 852-859.
Giovannucci, E.; Ascherio, A.; Rimm, E.B.; Stampfer, M.J.; Colditz, G.A.;
Willett, W.C. 1995: Intake of carotenoids and retinol in relation to risk of
prostate cancer. Journal of the National Cancer Institute 87: 1767-1776.
Giovannucci, E.; Ascherio A.; Rimm E.B.; Stampfer M.J.; Colditz G.A.; Willett
W.C. 2002: A prospective study of tomato products, lycopene and prostate
cancer risk. Journal of the National Cancer Institute 94(5): 391-398.
Giovannucci, E. 2003: Tomatoes, lycopene and prostate cancer. Inhouse
Pharmacy. www.inhousepharmacy.com
Gomez, R.; Costa, J.; Amo, M., Alvarruiz, A.; Picazo, M.; Pardo, J.E. 2001:
Physicochemical and colorimetric evaluation of local varieties of tomato
grown in SE Spain. Journal of the Science of Food and Agriculture 81(11):
1101-1105.
Page 55

Goodman, M.T.; Kiviat, N.; McDuffie, K.; Hankin, J.H.; Hernandez, B.;
Wilkens, L.R.; Franke, A.; Kuypers, J.; Kolonel, L.N.; Nakamura, J.; Ing, G.;
Branch, B.; Bertram, C.C.; Kamemoto, L.; Sharma, S.; Killeen, J. 1998: The
association of plasma micronutrients with the risk of cervical dysplasia in
Hawaii. Cancer Epidemiology Biomarkers & Prevention 7: 347-350.
Graefe, E.U.; Wittig, J.; Mueller, S.; Riethling, A.K.; Uehleke, B.; Drewelow,
B.; Pforte, H.; Jacobasch, G.; Derendorf, H.; Veit, M. 2001: Pharmacokinetics
and bioavailability of quercetin glycosides in humans. Journal of Clinical
Pharmacology 41(5): 492-499.
Gross, J. 1991: Pigments in vegetables. Chlorophylls and carotenoids. Van
Nostrand Reinhold, New York. Pp. 85, 242-247.
Hamner, K.C.; Bernstein, L.; Maynard, L.A. 1945: Effects of light intensity,
day length, temperature, and other environment factors on the ascorbic acid
content of tomatoes. Journal of Nutrition 29: 85-97.
Harbourne, J.B. 1993: The flavonoids: advances in research since 1986.
London, Chapman and Hall.
Hart, D.J.; Scott, K.J. 1995: Development and evaluation of an HPLC method
for the analysis of carotenoids in foods, and the measurement of the
carotenoid content of vegetables and fruits commonly consumed in the UK.
Food Chemistry 54: 101-111.
Hayes, R.B.; Ziegler, R.G.; Gridley, G.; Swanson, C.; Greenberg, R.S.;
Swanson, G.M.; Schoenberg, J.B.; Silverman, D.T.; Brown, L.M.; Pottern,
L.M.; Liff, J.; Schwartz, A.G.; Fraumeni, J.F. Jr.; Hoover, R.N. 1999: Dietary
factors and risks for prostate cancer among blacks and whites in the United
States. Cancer Epidemiology Biomarkers & Prevention 8(1): 25-34.
Hayman, G. 1999: Horticultural Development Council Research Report PC
167. [cited in Tomatoes and Health, British Tomato Growers Association,
www.britishtomatoes.co.uk]
Head, K.A. 1999: Natural therapies for ocular disorders, part one: diseases of
the retina. Alternative Medicine Reviews 4(5): 342-359.
Head, K.A. 2001: Natural therapies for ocular disorders, part two: cataracts
and glaucoma. Alternative Medicine Reviews 6(2): 141-166.
Hecht, S.S.; Kenney, P.M.; Wang, M.; Trushin, N.; Argawal, S.; Rao, A.V.;
Upadhyaya, P. 1999: Evaluation of butylated hydroxyanisole, myo-inositol,
curcumin, esculetin, resveratrol and lycopene as inhibitors of benzo[a]pyrene
plus 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumori-
genesis in A/J mice. Cancer Letters 137(2): 123-130.
Helzlsouer, K.J.; Comstock, G.W.; Morris, J.S. 1989: Selenium, lycopene,
alpha-tocopherol, beta-carotene, retinol, and subsequent bladder cancer.
Cancer Research 49(21): 6144-6148.
Herrmann, K. 1973: The phenolics of fruits. I. Our knowledge of occurrence
and concentrations of fruit phenolics and of their variations in the growing
fruit. Zeitschrift fur Lebensmittel-Untersuchung und -Forschung 151: 141.
Hertog, M.G.L.; Hollman, P.C.H.; Katan, M.B. 1992: Content of potentially
anticarcinogenic flavonoids of 28 vegetables and 9 fruits commonly
Page 56

consumed in the Netherlands. Journal of Agricultural and Food Chemistry 40:
2379-2383.
Hobson, G.; Davies, J. 1971: The tomato. In: Hulme, A.C. ed. Biochemistry of
fruits and their products. Norwich, UK, Academic Press. Vol 2. Pp. 453-457.
Holden, J.M.; Eldridge, A.L.; Beecher, G.R.; Buzzard, I.M.; Bhagwat, S.A.;
Davis, C.S.; Douglass, Larry W.; Gebhardt, S.E.; Haytowitz, D.B.; Schakel, S.
1999: Carotenoid Content of U.S. Foods: An Update of the Database. Journal
of Food Composition and Analysis 12: 169-196.
Holick, C.N.; Michaud, D.S.; Stolzenberg-Solomon, R.; Mayne, S.T.; Pietinen,
P.; Taylor, P.R.; Virtamo, J.; Albanes, D. 2002: Dietary carotenoids, serum
beta-carotene, and retinol and risk of lung cancer in the alpha-tocopherol,
beta-carotene cohort study. American Journal of Epidemiology 156(6): 536-
547.
Hoogwerf, B.J.; Young, J.B. 2000: The HOPE study. Ramipril lowered
cardiovascular risk, but vitamin E did not. Cleveland Clinic Journal of
Medicine 67(4): 287-293.
Hsing, A.W.; Comstock, G.W.; Abbey, H.; Polk, B.F. 1990: Serologic
precursors of cancer. Retinol, carotenoids, and tocopheral and risk of
prostate cancer. Journal of the National Cancer Institute 82: 941-946. [cited
Giovannucci 1995]
Hunt, G.M.; Baker, E.A. 1980: Phenolic constituents of tomato fruit cuticles.
Phytochemistry 19: 1415-1419.
Jarvinen, R.; Knekt, P.; Seppanen, R.; Teppo, L. 1997: Diet and breast
cancer risk in a cohort of Finnish women. Cancer Letters 114(1-2): 251-253.
Jian, L.; Du, C.J.; Lee, A.H.; Binns, C.W. 2005: Do dietary lycopene and
other carotenoids protect against prostate cancer? International Journal of
Cancer 113: 1010-1014.
Johnson, E.J. 1998: Human studies on bioavailability and plasma response
of lycopene. Proceedings of the Society for Experimental Biology and
Medicine 218(2): 115-120.
Johnson, E.J.; Qin, J.; Krinsky, N.I.; Russell, R.M. 1997: Ingestion by men of
a combined dose of beta-carotene and lycopene does not affect the
absorption of beta-carotene but improves that of lycopene. Journal of
Nutrition 127(9): 1833-1837.
Kalt, W. 2001: Health functional phytochemicals of fruit. Horticultural Reviews
27: 269-315.
Kanetsky, P.A.; Gammon, M.D.; Mandelblatt, J.; Zhang, Z.F.; Ramsey, E.;
Dnistrian, A.; Norkus, E.P.; Wright, T.C. Jr. 1998: Dietary intake and blood
levels of lycopene: association with cervical dysplasia among non-hispanic,
black women. Nutrition and Cancer 31: 31-40.
Kerkhofs, N.S. 2003: An investigation of the influence of air-drying on the
antioxidant components and antioxidant activity of New Zealand grown
tomatoes. BSc Hons dissertation, Lincoln, Lincoln University. 85 p.
Page 57

Key, T.J.A.; Silcocks, P.B.; Davey, G.K.; Appelby, P.N.; Bishop, D.T. 1997: A
case-control study of diet and prostate cancer. British Journal of Cancer
76(5): 678-687.
Khachik, F.; Carvalho, L.; Bernstein, P.S.; Muir, G.J.; Zhao, D.Y.; Katz, N.B.
2002: Chemistry, distribution, and metabolism of tomato carotenoid and their
impact on human health. Experimental Biology and Medicine (Maywood)
227(10): 845-851.
Kim, D.J.; Takasuka, N.; Nishino, H.; Tsuda, H. 2000: Chemoprevention of
lung cancer by lycopene. Biofactors 13(1-4): 95-102.
Klein, E.A.; Thompson, I.M. 2004: Update on chemoprevention of prostate
cancer. Current opinion in urology 141:143-149
Kohlmeier, L.; Kark, J.D.; Gomez-Gracia, B.; Martin, B.C.; Steck, S.E.;
Kardinaal, A F, Ringstad, J.; Tharamni, M.; Masaev, V.; Reimersma, R.;
Marin-Moreno, J.M.; Huttunen, J.K.; Kok, F.J. 1997: Lycopene and
myocardial infarction risk in the EURAMIC study. American Journal of
Epidemiology 146: 618-626.
Kotake-Nara, E.; Kushiro, M.; Zhang, H.; Sugawara, T.; Miyashita, K.; Nagao,
A. 2001: Carotenoids affect proliferation of human prostate cancer cells.
Journal of Nutrition 131(12): 3303-3306.
Krinsky, N.I. Cornwell, D.G.; Oncley, J.L. 1958: The transport of vitamin A
and carotenoids in human plasma. Archives of Biochemistry and Biophysics
73: 233-246.
Kristenson, M.; Zieden, B.; Kucinskiene, Z.; Elinder, L.S.; Bergdahl, B.;
Elwing, B. 1997 Antioxidant state and mortality from coronary heart disease
in Lithuanian and Swedish men: concomitant cross sectional study of men
aged 50. British Medical Journal 314: 629-633.
Kucuk, O.; Sarkar, F.H.; Sakr, W.; Djuric, Z.; Pollak, M.N.; Khachik, F.; Li,
Y.W.; Banerjee, M.; Grignon, D.; Bertram, J.S.; Crissman, J.D.; Pontes, E.J.;
Wood, D.P. Jr. 2001: Phase II randomized clinical trial of lycopene
supplementation before radical prostatectomy. Cancer Epidemiology
Biomarkers & Prevention 10(8): 861-868.
Kühnau J. 1976: The flavonoids: a class of semi-essential food components:
their role in human nutrition. World Review of Nutrition and Dietetics 24: 117-
191.
Lacatus, V.; Botez, C.; Popescu, N.; Voican, V. 1995: Chemical composition
of tomato and sweet pepper fruits cultivated on active substrates. Acta
Horticulturae 412: 168-175.
Lecomte, E.; Grolier, P.; Herbeth, B.; Pirollet, P.; Musse, N.; Paille, F.;
Braesco, V.; Siest, G.; Artur, Y. 1994: The relation of alcohol consumption to
serum carotenoid and retinol levels. Effects of withdrawal. International
Journal for Vitamin and Nutrition Research 64(3): 170-175.
La Vecchia, C. 2002: Tomatoes, lycopene intake, and digestive tract and
female hormone-related neoplasms. Experimental Biology and Medicine
(Maywood) 227(10): 860-863.
Page 58

Le Marchand, L.; Hankin, J.H.; Kolonel, L.N.; Wilkens, L.R.; 1991 Vegetable
and fruit consumption in relation to prostate risk in Hawaii: a reevaluation of
the effect of beta carotene. American Journal of Epidemiology 133: 215-219.
Leonardi, C.; Ambrosino, P.; Esposito, F.; Fogliano, V. 2000: Antioxidative
activity and carotenoid and tomatine contents in different typologies of fresh
consumption tomatoes. Journal of Agricultural and Food Chemistry 48(10):
4723-4727.
Levi, F.; Pasche, C.; Lucchini, F.; La Vecchia, C. 2001: Dietary intake of
selected micronutrients and breast cancer risk. International Journal of
Cancer 91: 260-263.
Levy, J.; Bosin, E.; Feldmen, B.; Giat, Y.; Miinster, A.; Danilenko, M. 1995:
Lycopene is a more potent inhibitor of human cancer cell proliferation than
either -carotene or β-carotene. Nutrition and Cancer 24(3): 257-266.
Libby, P.; Ridker, P.M. 1999: Novel inflammatory markers of coronary risk:
theory versus practice. Circulation 100(11): 1148-1150.
Liptay, A.; Papadopoulos, A.P.; Bryan, H.H.; Gull, D. 1986: Ascorbic acid
levels in tomato (Lycopersicon esculentum Mill) at low temperatures.
Agricultural and Biological Chemistry 50(12): 3185-3187. [cited in Dumas et
al. 2003]
Lister, C.E. 2003: Antioxidants: a health revolution. Christchurch, New
Zealand, New Zealand Institute for Crop & Food Research Limited.
Livny, O.; Kaplan, I.; Reifen, R.; Polak-Charcon, S.; Madar, Z.; Schwartz, B.
2002: Lycopene inhibits proliferation and enhances gap-junction
communication of KB-1 human oral tumor cells. Journal of Nutrition 132(12):
3754-3759.
London, S.J.; Stein; E.A.; Henderson, I.C.; Stampfer, M.J.; Wood, W.C.;
Remine, S.; Dmochowski, J.R.; Robert, N.J.; Willet, W.C. 1992: Carotenoids,
retinol and vitamin E and risk of proliferative benign breast disease and
breast cancer. Cancer Causes & Control 3: 503-512.
Lu Q-U.; Hung, J-C.; Heber, D.; Go, V.L.W.; Reuter, V.E.; Cordon-Cardo, C.;
Scher, H.I.; Marshal, J.R.; Zhang, Z. 2001: Inverse associations between
plasma lycopene and other carotenoids and prostate cancer. Cancer
Epidemiology Biomarkers & Prevention 10(7): 749-756.
McCollum, J.P. 1954: Effects of light on the formation of carotenoids in
tomato fruits. Food Research 19: 182-189.
Macheix, J.-J.; Fleuriet, A.; Billot, J. 1990: Fruit phenolics. CRC Press, Boca
Raton, Florida.
Macquart-Moulin, G.; Riboli, E.; Cornee, J.; Charnay, B.; Berthezene, P.;
Day, N. 1986: Case-control study on colorectal cancer and diet in Marseilles.
International Journal of Cancer 38(2): 183-191.
Macrae, R.; Robinson, R.K.; Sadler, M.J. 1993: Encyclopaedia of food
science, food technology and nutrition. London, Academic Press.
Manzano, N.T. 2001: Farmacy tomato. Tomate de farmacia. Agroanalysis
21(10): 36-38.
Page 59

Mares-Perlman, J.A.; Brady, W.E.; Klein, R.; Klein, B.E.; Bowen, P.;
Stacewicz-Sapuntzakis, M.; Palta, M. 1995: Serum antioxidants and age-
related macular degeneration in a population-based case-control study.
Archives of Ophthalmology 113(12): 1518-1523.
Martinez-Valverde, I.; Periago, M.J.; Provan, G.; Chesson, A. 2002: Phenolic
compounds, lycopene and antioxidant activity in commercial varieties of
tomato (Lycopersicon esculentum). Journal of the Science of Food and
Agriculture 82: 323-330.
Matsuzoe, N.; Zushi, K.; Johjima, T. 1998: Effect of soil water deficit on
coloring and carotene formation in fruits of red, pink and yellow type cherry
tomatoes. Journal of the Japanese Society Horticultural Science 67(4): 600-
606.
Meltzer, G.E.; Kravets, B.Z. 1998: Diet, nutrition, and diseases of the eye.
Journal of Applied Nutrition 50: 17-47.
Michaud, D.S.; Augustsson, K.; Rimm, E.B.; Stampfer, M.J.; Willet, W.C.;
Giovannucci, E. 2001: A prospective study on intake of animal products and
risk of prostate cancer. Cancer Causes and Control 12(6): 557-567.
Mills, P.K.; Beeson, W.L.; Phillips, R.L.; Fraser, G.E.1989: Cohort study of
diet and lifestyle and prostate cancer in Adventist men. Cancer 64: 598-604.
[cited in Giovannucci et al. 1995]
Minoggio, M.; Bramati, L.; Simonetti, P.; Gardana, C.; Iemoli, L.; Santagelo,
E.; Mauri, P.L.; Spigno, P.; Soressi, G.P.; Pietta, P.G. 2003: Polyphenol
pattern and antioxidant activity of different tomato lines and cultivars. Annals
of Nutrition and Metabolism 47(2): 64-69.
Modan, B.; Cuckle, H.; Lubin, F. 1981: A note on the role of dietary retinol
and carotene in human gastro-intestinal cancer. International Journal of
Cancer 28(4): 421-424.
Molyneux, S. 2001: The influence of cultivar and storage on the antioxidant
capacity, and the antioxidant content, of locally grown tomatoes. BSc(Hons)
thesis, Lincoln University, Lincoln, Canterbury.
Montagu, K.D.; Goh, K.M. 1990: Effects of forms and rates of organic and
inorganic nitrogen fertilizers on the yield and some quality indices of
tomatoes (Lycopersicon esculentum Miller). New Zealand Journal of Crop
and Horticultural Science 18: 31-37.
Moretti, C.L.; Sargent, S.A.; Huber, D.J.; Calbo, A.G.; Puschmann, R. 1998:
Chemical composition and physical properties of pericarp, locule, and
placental tissues of tomatoes with internal bruising. Journal of American
Society for Horticultural Science 123(4): 656-660.
Morris, D.L.; Kritchevsky, S.B.; Davis, C.E. 1994: Serum carotenoids and
coronary heart disease: the Lipid Research Clinics Coronary Primary
Prevention Trial and Follow-up Study. JAMA 272: 1439-1441.
Mortensen, A.; Skibsted, L.H. 1997: Relative stability of carotenoid radical
cations and homologue tocopheroxyl radicals. A real time kinetic study of
antioxidant hierarchy. FEBS Letters 417: 261-266. [cited in Argawal & Rao
2000]
Page 60

Murneek, A.E.; Maharg, L.; Wittwer, S.H. 1954: Ascorbic acid (vitamin C)
content of tomatoes and apples. University of Missouri Agriculture
Experimental Station Research Bulletin 568: 3-24. [cited in Dumas et al.
2003]
Nagasawa, H.; Mitamura, T.; Sakamoto, S.; Yamamoto, K. 1995: Effects of
lycopene on spontaneous mammary tumour development in SHN virgin mice.
Anticancer Research 15: 1173-1178.
Naphade, A.S. 1993: Effect of water regime on the quality of tomato.
Maharashtra Journal of Horticulture 7(2): 55-60.
Nardini, M.; Cirillo, E.; Natella, F.; Scaccini, C. 2002: Absorption of phenolic
acids in humans after coffee consumption. Journal of Agricultural and Food
Chemistry 50(20): 5735-5741.
Nguyen, M.L.; Schwartz, S.J. 1998: Lycopene stability during food
processing. Proceedings of the Society for Experimental Biology and
Medicine 218: 101-105.
Nguyen, M.L.; Schwartz, S.J. 1999: Lycopene: chemical and biological
properties. Food Technology 53: 38-45.
Nomura, A.M.Y.; Stemmerman, G.N.; Lee, J. Craft, N.E. 1997: Serum
micornutrients and proste cancer in Japanese Americans. Cancer
Epidemiology Biomarkers & Prevention 6: 487-491. [cited Giovannucci 1995]
Norrish, A.E.; Jackson, R.T.; Sharpe, S.J.; Skeaf, C.M. 2000, Prostate and
dietary carotenoids. American Journal of Epidemiology 151(2): 119-123.
Okajima, E.; Ozono, S.; Endo, T.; Majima, T.; Tsutsumi, M.; Fukuda, T.; Akai,
H.; Denda, A.; Hirao, Y.; Okajima, E.; Nishino, H.; Nir, Z.; Konishi, Y. 1997:
Chemopreventive efficacy of piroxicam administered alone or in combination
with lycopene and beta-carotene on the development of rat urinary bladder
carcinoma after N-butyl-N-(4-hydroxybutyl)nitrosamine treatment. Japanese
Journal of Cancer Research 88(6): 543-552.
Orlowski, M; Grzeszczuk, M; Gorecka, K. 2002: Evaluation of the fruit
biological value of small fruity tomato cherry type grown in unheated high
plastic tunnel. Vegetable Crops Research Bulletin 54(2): 21-24.
Paiva, E.A.S.; Sampaio, R.A.; Martinex, H.E.P. 1998: Composition and
quality of tomato fruit cultivated in nutrient solutions containing different
calcium concentrations. Journal of Plant Nutrition 21(12): 2653-2661.
Pantos, C.E.; Markakis, P. 1973: Ascorbic acid content of artificially ripened
tomatoes. Journal of Food Science 38: 550.
Parr, A.J.; Bolwell, U.P. 2000: Phenols in the plant and in man. The potential
for possible nutritional enhancement of the diet by modifying the phenols
content or profile. Journal of the Science of Food and Agriculture 80: 985-
1012.
Pastori, M.; Pfander, H.; Bosacoboinik, D. Azzi, A. 1998: Lycopene in
association with alpha-tocopherol inhibits at physiologicla concentrtions
prfoliferation of prosteate carcinoma cells. Biochemical and Biophysical
Research Communications 250: 582-585.
Page 61

Periquet, B.A.; Jammes, N.M.; Lambert, W.E.; Tricoire, J.; Moussa, M.M.;
Garcia, J.; Ghisolfi, J.; Thouvenot, J. 1995: Micronutrient levels in HIV-1-
infected children. AIDS 9(8): 887-893.
Polidori, M.C.; Mecocci, P.; Stahl, W.; Parente, B.; Cecchetti, R.; Cherubini,
A.; Cao, P.; Sies, H.; Senin, U. 2000: Plasma levels of lipophilic antioxidants
in very old patients with type 2 diabetes. Diabetes-Metabolism Research and
Reviews 16: 15-19.
Pollack, A.; Madar, Z.; Eisner, Z.; Nyska, A.; Oren, P. 1996: Inhibitory effect
of lycopene on cataract development in galactosemic rats. Metabolic
Pediatric and Systemic Ophthalmology 19-20: 31-36.
Porrini, M.; Riso, P.; Testolin, G. 1998: Absorption of lycopene from single or
daily portions of raw and processed tomato. British Journal of Nutrition 80(4):
353-361.
Potischman, N.; Herrero, R.; Brinton, L.A.; Reeves, W.C.; Stacewicz-
Sapuntzakis, M.; Jones, C.J.; Brenes, M.M.; Tenorio, F.; de Britton, R.C.;
Gaitan, E. 1991: A case-control study of nutrient status and invasive cervical
cancer. II. Serologic indicators. American Journal of Epidemiology 134(11):
1347-1355.
Potischman, N.; Hoover, R.N.; Brinton, L.A.; Swanson, C.A.; Herrero, R.;
Tenorio, F.; de Britton, R.C.; Gaitan, E.; Reeves, W.C. 1994: The relations
between cervical cancer and serological markers of nutritional status.
Nutrition and Cancer 21(3): 193-201.
Potischman, N.; McCulloch, C.E.; Byers, T.; Nemoto, T.; Stubbe, N.; Milch,
R.; Parker, R.; Rasmussen, K.M.; Root, M.; Graham, S.; Campbell, T.C.
1990: Breast cancer and dietary and plasma concentrations of carotenoids
and vitamin A. American Journal of Clinical Nutrition 52(5): 909-915.
Ramon, J.M.; Serra, L.; Cerdo, C.; Oromi, J. 1993: Dietary factors and gastric
cancer risk. A case-control study in Spain. Cancer 71(5): 1731-1735.
Rao, A.V. 2002: Lycopene, tomatoes, and the prevention of coronary heart
disease. Experimental Biology and Medicine (Maywood) 227(10): 908-913.
Rao, A.V.; Agarwal, S. 1999: Role of lycopene as an antioxidant carotenoid in
the prevention of chronic disease: a review. Nutrition Research 19(2): 305-
323.
Rao, A.V.; Agarwal, S. 2000: Role of lycopene in cancer and heart disease.
Journal of the American College of Nutrition 19(5): 563-569.
Rao, A.V.; Fleshner, N.; Agarwal, S. 1999: Serum and tissue lycopene and
biomarkers of oxidation in prostate cancer patients: a case control study.
Nutrition and Cancer 33: 159-164.
Rao, A.V.; Waseem, Z.; Agarwal, S. 1998: Lycopene contents of tomatoes
and tomato products and their contribution to dietary lycopene. Food
Research International 31: 737-741.
Re, R.; Bramley, P.M.; Rice-Evans, C. 2002: Effects of food processing on
flavonoids and lycopene status in a Mediterranean tomato variety. Free
Radical Research 36(7): 803-810.
Page 62

Rechner, A.R.; Kuhnle, G.; Hu, H.; Roedig-Penman, A.; van den Braak, M.H.;
Moore, K.P.; Rice-Evans, C.A. 2002: The metabolism of dietary polyphenols
and the relevance to circulating levels of conjugated metabolites. Free
Radical Research 36(11): 1229-1241.
Reddy, P.P.; Clevidence, B.A.; Berlin, E.; Taylor, P.R.; Bieri, J.G.; Smith, J.C.
1989: Plasma carotenoids and vitamin E profile of lipoprotein fractions of men
fed a controlled typical U.S. diet. FASEB Journal 3: A955.
Ribaya-Mercado, J.D.; Garmyn, M.; Gilchrest, B.A.; Russell, R.M. 1995: Skin
lycopene is destroyed preferentially over beta-carotene during ultraviolet
irradiation in humans. Journal of Nutrition 125(7): 1854-1859.
Rice-Evans, C.; Spencer, J.P.; Schroeter, H.; Rechner, A.R. 2000:
Bioavailability of flavonoids and potential bioactive forms in vivo. Drug
Metabolism and Drug Interactions 17(1-4): 291-310.
Richelle, M.; Bortlik, K.; Liardet, S.; Hager, C.; Lambelet, P.; Baur, M.;
Applegate, L.A.; Offord, E.A. 2002: A food-based formulation provides
lycopene with the same bioavailability to humans as that from tomato paste.
Journal of Nutrition 132: 404-408.
Rimm, E.B.; Stampfer, M.J.; Ascherio, A.; Giovannucci, E.; Colditz, G.A.;
Willett, W.C. 1993: Vitamin E consumption and the risk of coronary heart
disease in men. New England Journal of Medicine 328: 1450-1456.
Rissanen, T.H.; Voutilainen, S.; Nyyssonen, K.; Salonen, R.; Kaplan, G.A.;
Salonen, J.T. 2003: Serum lycopene concentrations and carotid
atherosclerosis: the Kuopio Ischaemic Heart Disease Risk Factor Study.
American Journal of Clinical Nutrition 77(1): 133-138.
Rock, C.L.; Swendseid, M.E. 1992: Plasma beta-carotene response in
humans after meals supplemented with dietary pectin. American Journal of
Clinical Nutrition 55(1): 96-99.
Ross, J.A.; Kasum, C.M. 2002: Dietary flavonoids: bioavailability, metabolic
effects, and safety. Annual Review of Nutrition 22: 19-34.
Ross, R. 1993: The pathogenesis of atherosclerosis: a perspective for the
1990s. Nature 362(6423): 801-809.
Rymal, K.S.; Nakayama, T.O.M. 1974: Major carotenoids of the seeds of
three cultivars of the tomato. Journal of Agricultural and Food Chemistry 22:
715-717.
Saini, S.P.S.; Singh, S. 1994: Juice composition of some new tomato hybrids.
Journal of Food Science and Technology (Mysore) 31(3): 231-232.
Saito, S.; Kano, F.J. 1970: Influence of nutrients on growth of solanaceous
vegetable plants, quality and chemical composition in their fruit. (part 1) On
the effect of different phosphate levels on the lycopene content of tomatoes.
Journal of Agricultural Science Tokyo 14: 233-238. [cited in Dumas et al.
2003]
Sanderson, M.J.; White, K.L.; Drake, I.M.; Schorah, C.J. 1997: Vitamin E and
carotenoids in gastric biopsies: the relation to plasma concentrations in
patients with and without Helicobacter pylori gastritis. American Journal of
Clinical Nutrition 65(1): 101-106.
Page 63

Scalbert, A.; Williamson, G. 2000: Dietary intake and bioavailability of
polyphenols. Journal of Nutrition 130: 2073S-2085S.
Schmitz, H.H.; Poor, C.L.; Wellman, R.B.; Erdman, J.W. Jr. 1991:
Concentrations of selected carotenoids and vitamin A in human liver, kidney
and lung tissue. Journal of Nutrition 121(10): 1613-1621.
Schuman, L.M.; Mandel, J.S.; Radke, A.; Seal, U.; Halberg, F. 1982: Some
selected features of the epidemiology of the prostatic cancer: Minneapolis-St.
Paul, Minnesota case-control study, 1979-96. In: Magnus, K. ed. Trends in
cancer incidence: causes and practical implications. Washington DC,
Hemisphere Publishing Corp. Pp. 345-354.
Schuurman, A.G.; Goldbohm, R.A.; Brants, H.A.; van den Brandt, P.A. 2002:
A prospective cohort study on intake of retinol, vitamins C and E, and
carotenoids and prostate cancer risk (Netherlands). Cancer Causes and
Control 13(6): 573-582.
Schierle, J.; Bretzel, W.; Buhler, I.; Faccin, N.; Hess, D.; Steiner, K.; Schuep,
W. 1996: Content and isomeric ratio of lycopene in food and human blood
plasma. Food Chemistry 59(3): 459-465.
Schwartz, S.J.; Nguyen, M.L.; Ferruzzi, M.G.; Francis, D.M. 1999: Lack of
isomerization of all-E lycopene in different tomato varieties during thermal
processing and in vitro digestion. 12th International Carotenoid Symposium.
Poster 1A-7.
Scott, J.; Thurnham, D.I.; Hart, D.J.; Bingham, S.H.; Day, K. 1996: The
correlation between the intake of lutein, lycopene, and beta-carotene from
vegetables and fruits, and plasma concentrations in a group of women aged
50-65 years in the UK. British Journal of Nutrition 75: 409-418.
Semenkovich, C.F.; Heinecke, J.W. 1997: The mystery of diabetes and
atherosclerosis: time for a new plot. Diabetes 46(3): 327-334.
Sengupta, A.; Das, S. 1999: The anti-carcinogenic role of lycopene,
abundantly present in tomato. European Journal of Cancer Prevention 8(4):
325-330.
Senter, S.D.; Horvat, R.J.; Forbus, W.R. 1988: Quantitative variation of total
phenols in fresh market tomatoes at three stages of maturity. Journal of Food
Science 53(2): 639-640.
Senti, F.R.; Rizek, R.L. 1975: Nutrient levels in horticultural crops.
HortScience 10: 243-246.
Shahidi, F.; Naczk, M. 1995: Food phenolics: sources, chemistry, effects,
applications. Lancaster, PA, USA, Technomic Publishing Co.
Shahidi, F.; Wanasundara, P.K.J.P.D. 1992: Phenolic antioxidants. CRC
Critical Reviews in Food Science and Nutrition 32(1): 67-103.
Sharma, S.K.; Le Maguer, M. 1996: Lycopene in tomatoes and tomato pulp
fractions. Italian Journal of Food Science 8(2): 107-113.
Shi, J.; Le Maguer, M. 2000: Lycopene in tomatoes: chemical and physical
properties affected by processing. Critical Reviews in Food Science and
Nutrition 40(1): 1-42.
Page 64

Shi, J.X.; Le Maguer, M.; Liptay, A.; Wang, S.L. 1999: Chemical composition
of tomatoes as affected by maturity and fertigation practices. Journal of Food
Quality 22: 147-156.
Sies, H.; Stahl, W. 1998: Lycopene: antioxidant and biological effects and its
bioavailability in the human. Proceedings of the Society for Experimental
Biology and Medicine 218(2): 121-124.
Sies, H.; Stahl, W. 1999: Bioavailability of lycopene. Acta Horticulturae 487:
389-393.
Siler, U.; Barella, L.; Spitzer, V.; Schnorr, J.; Lein, M.; Goralczyk, R.; Wertz,
K. 2004: Lycopene and Vitamin E interfere with autocrine/paracrine loops in
the Dunning prostate cancer model. FASEB J.: 03-1116fje.
Stahl, W.; Heinrich, U.; Jungmann, H.; Sies, H.; Tronnier, H. 2000:
Carotenoids and carotenoids plus vitamin E protect against ultraviolet light-
induced erythema in humans. American Journal of Clinical Nutrition 71(3):
795-798.
Stahl, W.; Heinrich, U.; Wiseman, S.; Eichler, O.; Sies, H.; Tronnier, H. 2001:
Dietary tomato paste protects against ultraviolet light-induced erythema in
humans. Journal of Nutrition 131(5): 1449-1451.
Stahl, W.; Schwarz, W.; Sundquist, A.R.; Sies, H. 1992: cis-trans Isomers of
lycopene and beta-carotene in human serum and tissues. Archives of
Biochemistry and Biophysics 294: 173-177.
Stahl, W.; Sies, H. 1992: Uptake of lycopene and its geometrical isomers is
greater from heat-processed than from unprocessed tomato juice in humans.
Journal of Nutrition 122: 2161-2166.
Stahl, W.; Sies, H. 1996: Lycopene: A biologically important carotenoid for
humans? Archives of Biochemistry and Biophysics 336: 1-9.
Stahl, W.; Sies, H. 2002: Carotenoids and protection against solar UV
radiation. Skin Pharmacology and Applied Skin Physiology 15(5): 291-296.
Stevens, M.A.; Rick, C.M. 1986: Genetics and breeding; fruit quality. In:
Atherton, J.G.; Rudich, J. ed. The tomato crop, a scientific basis for
improvement. London, Chapman and Hall Ltd. Pp. 84-96.
Stewart, A.J.; Bozonnet, S.; Mullen, W.; Jenkins, G.I.; Lean, M.E.J.; Crozier,
A. 2000: Occurrence of flavonols in tomatoes and tomato-based products.
Journal of Agricultural and Food Chemistry 48(7): 2663-2669.
Subbiah, K.; Perumal, R. 1990: Effect of calcium sources, concentrations,
stages and numbers of sprays on physiochemical properties of tomato fruits.
South Indian Horticulture 38(1): 20-27. [cited in Dumas et al. 2003]
Tajima, K.; Tominaga, S. 1985: Dietary habits and gastro-intestinal cancers:
a comparative case-control study of stomach and large intestinal cancers in
Nagoya, Japan. Japanese Journal of Cancer Research 76(8): 705-716.
Takeoka, G.R.; Dao, L.; Flessa, S.; Gillespie, D.M.; Jewell, W.T.; Huebner,
B.; Bertow, D.; Ebeler, S. 2001: Processing effects on lycopene content and
antioxidant activity of tomatoes. Journal of Agricultural and Food Chemistry
49: 3713-3717.
Page 65

Terry, P.; Jain, M.; Miller, A.B.; Howe, G.R.; Rohan, T.E. 2002: Dietary
carotenoid intake and colorectal cancer risk. Nutrition and Cancer 42(2): 167-
172.
Thompson K.A.; Marshall M.R.; Sims C.A.; Wei C.I.;Sargent S.A.; Scott J.W.
2000: Cultivar, maturity and heat treatment on lycopene content in tomatoes.
Journal of Food Science 65(5): 791-795.
Tonucci, L.H.; Holden, J.M.; Beecher, G.R.; Khachik, F.; Davis, C.S.
Mulokozi, G. 1995: Carotenoid content of thermally processed tomato-based
food products. Journal of Agricultural and Food Chemistry 43: 579-586.
Toor, R.K.; Savage, G.P. 2005: Antioxidant activity in different fractions of
tomatoes. Food Research International 38: 487-494.
Trivedi, D.; Mohanty, I.; Srivastava, S.; Gupta, S.K. 2001a: Lycopene, a
natural antioxidant protects against cataractous changes in lens epithelial
cells. Indian Journal of Pharmacology 33(3): 241-242.
Trivedi, D.; Srivastava, S.; Gupta, S.K. 2001b: Prevention of cataract
development by lycopene: an experimental study. Indian Journal of
Pharmacology 33(3): 242.
Trudel, M.J.; Ozbun, J.L. 1971: Influence of potassium on carotenoid content
of tomato fruit. Journal of the American Society for Horticultural Science 96:
763-765.
Tsugane, S.; Tsuda, M.; Gey, F.; Watanabe, S. 1992: Cross-sectional study
with multiple measurements of biological markers for assessing stomach
cancer risks at the population level. Environmental Health Perspectives 98:
207-210.
Upritchard, J.E.; Sutherland, W.H.; Mann, J.I. 2000: Effects of
supplementation with tomato juice, vitamin E and vitamin C on LDL oxidation
and products of inflammatory activity in type 2 diabetes. Diabetes Care 23:
733-738.
van het Hof, K.H.; de Boer, B.C.J.; Tijburg, L.B.M.; Lucius, B.R.H.M.; Zijp, I.;
West, C.E.; Hautvast, J.G.A.J.; Weststrate, J.A. 2000: Carotenoid
bioavailability in humans from tomatoes processed in different ways
determined from the carotenoid response in the triglyceride-rich lipoprotein
fraction of plasma after a single consumption and in plasma after four days of
consumption. Journal of Nutrition 130: 1189-1196.
van het Hof, K.H.; West, C.E.; Weststrate, J.A.; Hautvast, J.G.A.J. 2000:
Dietary factors that affect the bioavailability of carotenoids. Journal of
Nutrition 130: 503-506.
Vegfed 2005: www.vegetables.co.nz, accessed 21/06/2005
Velmurugan, B.; Bhuvaneswari, V.; Nagini, S. 2002: Antiperoxidative effects
of lycopene during N-methyl-N’-nitro-N-nitrosoguanidine-induced gastric
carcinogenesis. Fitoterapia 73(7-8): 604-611.
Venter, F. 1977: Solar radiation and vitamin C content of tomato fruits. Acta
Horticulturae 58: 121-127.
Verhoeyen, M.E.; Bovy, A.; Collins, G.; Muir, S.; Robinson, S.; de Vos,
C.H.R.; Colliver, S. 2002: Increasing antioxidant levels in tomatoes through
Page 66

modification of the flavonoid biosynthetic pathway. Journal of Experimental
Botany 53(377): 2099-2106.
Virginia Tech 2003: courseware.vt.edu/users/welbaum/lesson/tomato
Vogt, T.M.; Mayne,S.T.; Graubard, B.I.; Swanson, C.A.; Sowell, A.L.;
Schoenberg, J.B.; Swanson, G.M.; Greenberg, R.S.; Hoover, R.N.; Hayes,
R.B.; Ziegler, R.G. 2002: Serum lycopene, other serum carotenoids and risk
of prostate cancer in U.S. Blacks and Whites. American Journal of
Epidemiology; 155(11): 1023-1032.
Wardale, D.A. 1973: Effect of phenolic compounds in Lycopersicon
esculentum on the synthesis of ethylene. Phytochemistry 12: 1523-1530.
Wilkens, R.T.; Spoerke, J.M.; Stamp, N.E. 1996: Differential responses of
growth and to soluble phenolics of tomato to resource availability. Ecology
77(1): 247-258.
Windsor, G.W. 1979: Some factors affecting the quality and composition of
tomatoes. Acta Horticulturae 93: 335-340.
Woldecke, M.; Herrmann, K. 1974: Flavonols and flavones of vegetables. III.
Flavonols and flavones of tomatoes and sweet pepper. Zeitschrift fur
Lebensmittel-Untersuchung und -Forschung 155(4): 216-219.
Woodall, A.A.; Lee, S.W.M.; Weesie, R.J.; Jackson, M.J.; Britton, G. 1997:
Oxidation of carotenoids by free radicals: relationship between structure and
reactivity. Biochimica and Biophysica Acta 1336: 33-42. [cited in Argawal &
Rao 2000]
Yamamoto, J.; Taka, T.; Yamada, K.; Ijiri, Y.; Murakami, M.; Hirata, Y.;
Naemura, A.; Hashimoto, M.; Yamashita, T.; Oiwa, K.; Seki, J.; Suganuma,
H.; Inakuma, T.; Yoshida, T. 2003: Tomatoes have natural anti-thrombotic
effects. British Journal of Nutrition 90: 1031-1038.
Yeum, K.J.; Russell, R.M. 2002: Carotenoid bioavailability and bioconversion.
Annual Review of Nutrition 22: 483-504.
Yeung, D.; Rao, V. 2001: Unlock the power of lycopene. Arpr inc, Pittsburg.
Zaripheh, S.; Erdman, J.W. Jr. 2002: Factors that influence the bioavailablity
of xanthophylls. Journal of Nutrition 132(3): 531-534.
Zhang, L.X.; Cooney, R.V.; Bertram, J.S. 1997: Carotenoids enhance gap
junctional communication and inhibit lipid peroxidation in C3H/10T1/2 cells:
relationship to their cancer chemopreventive action. Carcinogenesis
1991(12): 2109-2114.
Zhang, S.; Tang, G.; Russell, R.M.; Mayzel, K.A.; Stampfer, M.J.; Willet,
W.C.; Hunter, D.J. 1997: Measurement of retinoids in breast adiose tissue
and a comparison of concentrations in breast cancer cases and control
subjects. American Journal of Clinical Nutrition 66(3): 626-632.
Zushi, K.; Matsuzoe, N. 1998: Effect of soil water deficit on vitamin C, sugar,
organic acid, amino acid and carotene contents of large-fruited tomatoes.
Journal of the Japanese Society for Horticultural Science 67(6): 927-923.
Page 67

Page 68

Appendices
Appendix I Additional information of general interest
 The word ”tomato” comes from the Aztec, “tomatl”, which was used by
the Spanish explorers who originally took the fruit back to Europe. In
Italy, it was quickly adopted into local cuisine and was known as “pomo
d’oro”, or golden apple, which suggests that the first tomatoes there were
yellow. In France it was called “pomme d’amour” or love apple. This may
have been a corruption of the Italian or may have reflected the belief that
tomatoes had aphrodisiac powers. It was for the latter reason that
tomatoes were forbidden to women in some cultures! The botanical
name is Lycopersicon esculentum meaning “edible wolf peach”, which is
derived from the German name for deadly nightshade, a relative of the
tomato, which was believed to be used by witches to summon up
werewolves.
 Although almost a staple in Western diets today, tomatoes were
considered poisonous in some parts of Europe when early Spanish
explorers brought them to the old world from their native South America.
This belief was also held in North America, until, so the story goes, a
champion for the tomato cause, Colonel Robert Gibbon Johnson,
announced he would eat a bushel of tomatoes in front of the Boston
courthouse. Apparently a 2000 strong crowd arrived, expecting to
witness his demise, but to their amazement he lived and any remaining
doubts about the tomato were dramatically and conclusively put to rest.
 Tomatoes are unusual amongst foods in that their consumption is not
necessarily related to healthy eating choices. For example, whilst they
may be part of a salad (healthy choice), they could also be consumed, as
tomato sauce, along with fish and chips, French fries, pies or pizza (less
healthy choices) or as a tomato-based sauce in a pasta meal (neither
particularly healthy nor unhealthy). This makes it particularly interesting
for researchers, as many potentially confounding issues are removed.
 In the USA, tomatoes contribute the second most dietary vitamin C, after
citrus.
 “A world without tomatoes is like a string quartet without violins”. Laurie
Colwyn, Home Cooking
Page 69

Appendix II
Composition of various tomato products from the New Zealand Food
Composition Database
 Tomato-based pasta sauce
 Tomato sauce
 Tomato puree
 Tomato paste, salted
 Tomatoes, flesh, skin and seeds, raw
Page 70

SAUCE, PASTA,TOMATO-BASED, commercial, heated
Amount in 100 g edible portion Units Mean Std Error No.
Src.
PROXIMATES
Water....................................................................................................... g 85.35 - 1
................................................................................................................z
Energy..................................................................................................... kcal 50 - -
................................................................................................................c
Energy..................................................................................................... kJ 205 - -
................................................................................................................c
Protein (Nitrogen x 5.8)......................................................................... g 1.4 - -
................................................................................................................a
Total fat................................................................................................... g 0.7 - -
................................................................................................................a
Carbohydrate, available......................................................................... g 9.4 - -
................................................................................................................a
Dietary fibre (Englyst, 1988) ................................................................ g 0.6 - -
............................................................................................................... b
Ash.......................................................................................................... g 1.4 - -
................................................................................................................a
NUTRIENT ELEMENTS
Sodium.................................................................................................... mg 470 - -
................................................................................................................a
Magnesium ............................................................................................. mg 17 - -
................................................................................................................a
Phosphorus ............................................................................................. mg 30 - -
................................................................................................................a
Sulphur.................................................................................................... mg - - -
................................................................................................................ -
Chloride .................................................................................................. mg 830 - -
............................................................................................................... b
Potassium................................................................................................ mg 360 - -
................................................................................................................a
Calcium................................................................................................... mg 24 - -
................................................................................................................a
Manganese.............................................................................................. µg 0.10 - -
............................................................................................................... b
Iron.......................................................................................................... mg 1.0 - -
................................................................................................................a
Copper .................................................................................................... mg 0.16 - -
............................................................................................................... b
Zinc ......................................................................................................... mg 0.25 0.08 10
................................................................................................................z
Selenium ................................................................................................. µg T - -
............................................................................................................... g
VITAMINS
Retinol .................................................................................................... µg 1 - -
................................................................................................................a
Beta-carotene equivalents...................................................................... µg 260 - -
................................................................................................................a
Total vitamin A equivalents.................................................................. µg 44 - -
................................................................................................................a
Thiamin................................................................................................... mg 0.02 - -
................................................................................................................a
Riboflavin ............................................................................................... mg 0.06 - -
................................................................................................................a
Niacin...................................................................................................... mg 1.0 - -
................................................................................................................a
Page 71

Potential niacin from tryptophan .......................................................... mg 0.2 - -
..............................................................................................................ac
Vitamin B6 ............................................................................................. mg 0.06 - -
............................................................................................................... b
Pantothenate........................................................................................... mg 0 - -
............................................................................................................... b
Biotin ...................................................................................................... µg 0 - -
............................................................................................................... b
Folate, total ............................................................................................. µg 10 - -
............................................................................................................... b
Vitamin B12 ........................................................................................... µg 0 - -
............................................................................................................... b
Vitamin C ............................................................................................... mg 0 - -
................................................................................................................a
Vitamin D ............................................................................................... µg 0 - -
............................................................................................................... b
Alpha-tocopherol ................................................................................... mg - - -
................................................................................................................ -
Vitamin E ............................................................................................... mg 0 - -
............................................................................................................... p
OTHER LIPIDS
Cholesterol.............................................................................................. mg 0 - -
................................................................................................................a
g/100 g edible portion mg/g Nitrogen
AMINO ACIDS Mean Std Error No. Src. Mean Std Error No.
Src.
Isoleucine.................................................. - - - - - - -
.................................................................. -
Leucine ..................................................... - - - - - - -
.................................................................. -
Lysine ....................................................... - - - - - - -
.................................................................. -
Methionine ............................................... - - - - - - -
.................................................................. -
Cystine...................................................... - - - - - - -
.................................................................. -
Phenylalanine ........................................... - - - - - - -
.................................................................. -
Tyrosine.................................................... - - - - - - -
.................................................................. -
Threonine.................................................. - - - - - - -
.................................................................. -
Tryptophan ............................................... - - - - - - -
.................................................................. -
Valine........................................................ - - - - - - -
.................................................................. -
Arginine.................................................... - - - - - - -
.................................................................. -
Histidine ................................................... - - - - - - -
.................................................................. -
Alanine...................................................... - - - - - - -
.................................................................. -
Aspartic acid............................................. - - - - - - -
.................................................................. -
Glutamic acid ........................................... - - - - - - -
.................................................................. -
Glycine...................................................... - - - - - - -
.................................................................. -
Page 72

Proline....................................................... - - - - - - -
.................................................................. -
Serine........................................................ - - - - - - -
.................................................................. -
Hydroxyproline ........................................ - - - - - - -
.................................................................. -
Common Measure 1 cup, 258 g
FOODINFO New Zealand Institute for Crop & Food Research
1.S
Page 73

SAUCE, PASTA,TOMATO-BASED, commercial, heated
g/100 g edible portion g/100 g total fatty acids
FATTY ACIDS Mean Std Error No. Src. Mean Std Error No.
Src.
Total saturated fatty acids........................ 0.1 - - a - - -
.................................................................. -
Total monounsaturated fatty acids.......... 0.2 - - a - - -
.................................................................. -
Total polyunsaturated fatty acids............ 0.4 - - a - - -
.................................................................. -
Additional information (in 100 g edible portion) Units Mean Std Error No.
Scr.
Alcohol ................................................................................... g 0 - -
................................................................................................ a
Cadmium ................................................................................ µg 1.39 0.21 10
................................................................................................ z
Carbohydrate, available......................................................... g 9.4 - -
................................................................................................ a
Carbohydrate, total (by difference)....................................... g 11 - -
................................................................................................ c
Density.................................................................................... kg/l 1.03 - -
................................................................................................ z
Dietary fibre ........................................................................... g 1.8 - -
................................................................................................ a
Dry matter............................................................................... g 14.7 - 1
................................................................................................ z
Fructose .................................................................................. g 3.7 - -
...............................................................................................ac
Glucose ................................................................................... g 3.8 - -
...............................................................................................ac
Insoluble non-starch polysaccharides................................... g 0 - -
.............................................................................................. bc
Lactose.................................................................................... g 0 - -
................................................................................................ b
Lead ........................................................................................ µg 0.63 0.08 8
............................................................................................... zl
Maltose ................................................................................... g 0 - -
................................................................................................ b
Soluble non-starch polysaccharides...................................... g 0.6 - -
.............................................................................................. bc
Starch ...................................................................................... g 1.9 - -
................................................................................................ a
Sucrose.................................................................................... g T - -
................................................................................................ b
Total available sugars ............................................................ g 7.5 - -
................................................................................................ a
Total niacin equivalents......................................................... mg 1.2 - -
...............................................................................................ac
Total nitrogen ......................................................................... g 0.24 - -
...............................................................................................ac
Carbohydrate exchange......................................................... 0.94 - -
................................................................................................ c
FOODINFO New Zealand Institute for Crop & Food Research S35 V0.00 28 APR 2003
2.S
Page 74

SAUCE, TOMATO
Composite of Cerebos,Watties `Homestyle' and King tomato sauce.
Amount in 100 g edible portion Units Mean Std Error No.
Src.
PROXIMATES
Water....................................................................................................... g 69.54 - -
..............................................................................................................zc
Energy..................................................................................................... kcal 105 - -
................................................................................................................c
Energy..................................................................................................... kJ 432 - -
................................................................................................................c
Protein (Nitrogen x 5.8)......................................................................... g 1.07 - 1
................................................................................................................z
Total fat................................................................................................... g 0.10 - 1
................................................................................................................z
Carbohydrate, available......................................................................... g 24.87 - -
..............................................................................................................zc
Dietary fibre (Englyst, 1988) ................................................................ g 1.32 - 1
................................................................................................................z
Ash.......................................................................................................... g 2.36 - 1
................................................................................................................z
NUTRIENT ELEMENTS
Sodium.................................................................................................... mg 615.00 - 1
................................................................................................................z
Magnesium............................................................................................. mg 16.40 - 1
................................................................................................................z
Phosphorus ............................................................................................. mg 23.78 - 1
................................................................................................................z
Sulphur.................................................................................................... mg 18.86 - 1
................................................................................................................z
Chloride .................................................................................................. mg - - -
................................................................................................................ -
Potassium................................................................................................ mg 397.70 - 1
................................................................................................................z
Calcium................................................................................................... mg 20.50 - 1
................................................................................................................z
Manganese.............................................................................................. µg 151.70 - 1
................................................................................................................z
Iron.......................................................................................................... mg 1.35 - 1
................................................................................................................z
Copper .................................................................................................... mg 0.11 - 1
................................................................................................................z
Zinc......................................................................................................... mg 0.14 - 1
................................................................................................................z
Selenium ................................................................................................. µg 3.28 - 1
................................................................................................................z
VITAMINS
Retinol .................................................................................................... µg 15 - -
.............................................................................................................. zr
Beta-carotene equivalents...................................................................... µg 104.47 -