ArticlePDF Available

Abstract and Figures

The purpose of this report is to alert the foodservice industry, particularly the fast-food industry, of an emerging health issue. Considerable evidence has accumulated over the past two decades that heated cooking oils, especially polyunsaturated oils, may pose several types of health risks to consumers of fried foods and even people working near deep fat fryers. Heat degrades polyunsaturated fatty acids to toxic compounds; saturated and monounsaturated fatty acids are resistant to heat-induced degradation. Several types of diseases may be related to the exposure of humans to food- or air-borne breakdown products of heated oils including atherosclerosis, the forerunner to cardiovascular disease; inflammatory joint disease, including rheumatoid arthritis; pathogenic conditions of the digestive tract; mutagenicity and genotoxicity, properties that often signal carcinogenesis; and teratogenicity, the property of chemicals that leads to the development of birth defects. Factors that can contribute to improved oil stability, and therefore fewer health concerns, are briefly discussed. The literature reviewed raises serious questions concerning the willful addition of large amounts of polyunsaturated fatty acids into the human diet without accompanying measures to ensure the protection of these fatty acids against heat- and oxidative-degradation. It is hoped that this review will stimulate interest in the foodservice industry in this important area of potential health concern, and also foster the research and development activities necessary to reduce the exposure of humans to lipid oxidation products.
Content may be subject to copyright.
HEALTH
EFFECTS
OF
OXIDIZED HEATED OILS'
MARTIN GROOTVELD*, CHRISTOPHER J.L. SILWOOD*, PAUL ADDIS3
and
ANDREW CLAXSOP
2Department
of
Diabetes and Metabolic Medicine
St. Bartholomew
3
and the Royal
London
Hospital's School
of
Medicine and Dentistry
London
El
IBB
3Department
of
Food Science and Nutrition
University
of
Minnesota
St. Paul, Minnesota
551
08
BARTOLOME BONET SERRA
and
MARTA VIANA
Facultad de Ciencias Experimentales
y
Tkcnicas
Universidad de San Pablo Ceu
Madrid, Spain
Received
for
Publication April
30.
2001
Accepted
for
Publication August 22, 2001
ABSTRACT
The purpose
of
this report is to alert the foodsenice industry. particularly
the fast-food industry, of an emerging health issue. Considerable evidence has
accumulated over the past
two
decades that heated cooking oils, especially
polyunsaturated oils,
may
pose several types
of
health risks
to
consumers offn'ed
foods and even people working near deep fathers. Heat degrades polyunsatu-
rated fatty acids
to
toxic compounds; saturated and monounsaturated fatty acids
are resistant
to
heat-induced degradation. Several types
of
diseases
may
be
related
to
the exposure
of
humans to food-
or
air-borne breakdown products
of
heated oils including atherosclerosis, the forerunner to cardiovascular disease;
injlammatory joint disease, including rheumatoid arthritis; pathogenic conditions
of the digestive tract; mutagenicity and genotoxicity, properties that open signal
carcinogenesis; and teratogenicity, the property of chemicals that leads to the
development of birth defects. Factors that can contribute to improved oil
stability,
and
therefore fewer health concerns, are
briejly
discussed. The
literature reviewed raises serious questions concerning the willfisl addition of
large amounts of polyunsaturated fatty acids into the human diet without
accompanying measures
to
ensure the protection
of
these fatty acids against
'
This research
has
been supported in part
by
the Minnesota Agricultural Experiment Station
Author
to
whom all correspondence should be addressed. TEL: 612-624-7704; FAX: 612425-
5272; E-mail: paddisQumn.edu
Foodservice Research
International
13
(2001) 41-55.
All
Rights Reserved.
"Copyright
2001
by
Food
&
Nutrition Press, Inc., Trumbull. Connecticut.
41
42
M.
GROOTVELD
ETA.
heat- and oxidative-degradation.
It
is hoped that this review will stimulate
interest
in
the foodservice industry
in
this important area
of
potential health
concern,
and
also foster the research and development activities necessary to
reduce the exposure of humans to lipid oxidation products.
INTRODUCTION
The thermally-induced oxidation of glycerol-bound polyunsaturated fatty
acids (PUFAs) in foods and culinary oils during standard frying or cooking
episodes is a process that involves the prior generation of isomeric conjugated
hydroperoxydiene (CHPD) species. These CHPDs fragment to form alkoxyl
radicals that, in turn, undergo 8-scission to generate a wide range of aldehydic
products.
In
view of the extremely toxic nature of the aldehydic end-products
generated, the employment of PUFA-containing culinary oils for domestic or
commercial fryinghoking episodes poses health hazards that have recently
attracted much public and clinical interest.
Indeed, these cytotoxic agents have been implicated in the development and
progression of atherosclerosis (Steinberg and Wit-
1990)
and its associated
pathological sequelae such
as
ischemic heart disease and peripheral vascular
disease, and have also been shown to exert gastropathic (Jayaraj
et al.
1986),
pro-inflammatory (Benedetti
et al.
1990),
and genotoxicological (Esterbauer
1982)
properties. These phenomena are undoubtedly attributable to the extremely
high reactivity of aldehydes with critical biomolecules (e.g., thiols such
as
glutathione; DNA, forming covalently-modified base adducts; and the apolipo-
protein B component of low-density lipoprotein, altering its biological
characteristics.)
Two of the contributors of this paper,
M.
Grootveld and
A.
Claxson, have
recently reported the detection and quantification of PUFA-derived oxidation
products (notably aldehydes and their CHPD precursors)
in
culinary oils by high
resolution proton ('H) nuclear magnetic resonance
(NMR)
spectroscopy, a
virtually noninvasive multicomponent analytical technique (Claxson
et
uZ.
1994;
Haywood
et al.
1995).
The influence of episodes of thermal stressing (i.e., those
that simulate their domestic or commercial usage) on the generation, nature and
concentrations of such products was also evaluated in these studies. We have
also employed this technique to probe the
in
vivo
absorption, metabolism and
urinary excretion of typical aldehydic lipid oxidation products in experimental
animals
and found that such agents are indeed absorbed from the gut into the
systemic circulation, metabolized (primarily via the addition of glutathione
across their electrophilic carbon-carbon double bonds), and excreted in the urine
as
C-3 mercapturate conjugates (Grootveld
et al.
1998).
HEATED
OILS:
HEALTH EFFECTS
43
The foregoing findings are especially relevant in view of the trend toward
the use of vegetable oils,
as
a replacement for
animal
fats, for the purpose of
frying/cooking practices. Vegetable oils, even those which have been subjected
to hydrogenation, are more labile than animal-derived lard and tallow. However,
neither a return to animal-derived cooking fats nor hydrogenated vegetable oils
is likely to provide an acceptable alternative
as
both are problematic with regard
to health effects (Addis
et
al.
1995). The issue of
trans
fatty acids is currently
under intense investigation and a number of potential adverse health effects have
been reported (Addis and Warner 1991; Addis
et
al.
1995). Regarding
cholesterol oxidation in the frying process, it has been demonstrated that toxic
cholesterol oxidation products (COPs) readily form in heated tallow (Park and
Addis 1986a,b). Furthermore, levels of COPs in heated tallow were predictable
by the conductivity
of
the frying medium (Zhang and Addis 1991). Moreover,
samples of French-fries obtained daily from a fast-food restaurant over a one-
month time period displayed significant though variable levels of COPs,
including the highly atherogenic
30,
5a,
60-cholestane trio1 (Zhang and Addis
1991). COPs have been shown to occur
in
the plasma lipoproteins of fasted
humans (Addis
et
al.
1989) and in chylomicrons of human subjects fed a meal
rich in fat and COPs postprandially (Emanuel
et
al.
1991). A review of the
literature of the biological and health effects of COPs and other components of
thermally-stressed oils would be enormous and will not
be
attempted here.
Several reviews of this area have been published and are recommended to the
reader (Addis 1986; Addis
et
al.
1993, 1995; Guardiola
el
al.
1996).
In
response to these foregoing issues, a tallow-based frying and baking fat has been
developed by removing cholesterol and blending the cholesterol-free tallow with
corn oil, achieving
an
oil that tends to raise serum HDL while also lowering
serum LDL (Hayes 1996). Because
the
foregoing oil
is
not
produced with
catalytic hydrogenation,
trans
fatty acids would appear not to be a problem. The
significance of this development stems from the fact that
trans
(elaidic) fatty
acids interfere with the beneficial effects of both saturated and polyunsaturated
fatty acids
-
namely, raising HDL and lowering LDL, respectively (Sundram
et
al.
1997; Hayes 1996). The removal of cholesterol is
also
advantageous in
terms of reducing serum cholesterol
in
subjects consuming the tallowhrn oil
blend (Hayes 1996).
In the following sections of this communication we review the toxicological
hazards afforded by the ingestion of aldehydes present in thermally-stressed
and/or repeatedly-utilized PUFA-rich culinary oils, and address potential
methods to limit the production of these deleterious agents during routine frying
processes.
44
M.
GROOTVELD
ETAL.
Cardiovascular
Diseases
Peroxidation of PUFA components of low-density lipoprotein (LDL)
in vivo
stimulates the subsequent production of foam cells from macrophages, a crucial
stage in the pathogenesis of atherosclerosis (Addis and Warner 1991; Van
Hinsbergh 1984), and this oxidative modification occurs from the following
sequential steps: (1) generation of aldehydes from the decomposition of pre-
formed, PUFA-derived CHPDs; and (2) alteration of the apolipoprotein
B
(apo
B)
moiety’s structure via Maillard reactions involving the above carbonyl
compounds. Hoff
ef
al.
(1989) demonstrated that
4-hydroxy-trans-2-nonenal
(HNE), an a,P-unsaturated aldehyde arising from the autoxidation of PUFAs,
reacted with selected
amino
acids of apo
B,
rendering it susceptible to uptake by
the macrophage scavenger receptor. Apo
B
lysine residues are readily
derivatized by aldehydic CHPD fragmentation products (Jurgens
e?
al.
1987).
Therefore, subsequent to their
in
vivo
absorption, aldehydes present in
thermally/ oxidatively-stressed frying
oils
ingested in the diet will have the
ability to directly effect structural modification of the apo
B
component of LDL,
a process that induces the generation of foam cells from macrophages
-
the
hallmark of atherosclerosis.
Interestingly, Smith and Kummerow (1987) have demonstrated that the
dietary consumption of peroxidized culinary oils escalated the accumulation of
‘oxidized lipids’
in
macrophages and monocytes, and previous animal feeding
studies have shown that diets containing thermally-stressed, PUFA-rich oils are
more atherogenic than those containing corresponding unheated oils. More
recently, Staprans
ef
al.
(1996) conducted investigations
aimed
at evaluating the
ability of oxidized dietary lipids to accelerate the development of atherosclerosis
in New Zealand White rabbits and found that such a diet increased levels of fatty
streak lesions, a “fingerprint” of atherosclerosis, by 100% compared to unheated
oils. These findings clearly indicate that the consumption of PUFA-derived
oxidation products in the diet represents a hazard to human health. Furthermore,
Kritchevsky and Tepper (1967) provided evidence for the atherogenicity of
thermally-stressed PUFA-rich oils
as
early
as
1967. These researchers found that
heating corn oil [PUFA-content
=
57%
(w/w)] at 215C for a period of 20
min
substantially increased its atherogenicity, whereas the heating of olive oil [PUFA
content
=
9% (w/w)] in the same manner had no effect on its atherogenic
properties.
Figure 1 shows expanded regions of high resolution ‘H NMR spectra of a
corn (maize) oil sample acquired prior to and subsequent to heating at a
temperature of 180C for a period of
30
min.
The results in Fig. 1 clearly reveal
the generation of CHPDs and their aldehydic fragmentation products during the
subjection of a commonly-utilized PUFA-laden culinary oil to episodes of
thermal stressing according to standard frying practices. Therefore, it is likely
HEATED
OILS:
HEALTH EFFECTS
45
that consumption of foods subjected to standard frying procedures is a health
concern to the consumer, especially regarding cardiovascular disease.
,~""'"'l""'"'I'"'~''''l'~"~'"'I'"'~'""''''~''''
G--Z
on
85
8.0
75
70
85
80
55
ppm
FIG.
1.
PROTON ('H) NMR ANALYSIS OF LIPID OXIDATION PRODUCTS IN
Partial
(5.00-10.00
ppm) region
of
a onedimensional
'H NMR
spectrum
of
a sample
of
corn (maize)
oil
subjected
to
an episode
of
heating according
to
standard frying practices
(30
min at
180C). A
typical spectrum is shown. Abbreviations:
'H
nuclear labels
of
lipid oxidation products correspond
to
labeled protons in the accompanying molecular stlllctllres
([a,
cis,
trans-conjugated hydroxy-
peroxydiene; trans,transconjugated hydroxyperoxydiene;
[IIII,
cis,
rranr-conjugated
hydroxydiene;
N,
n-alkanal;
IV),
rrans-2-alkenal;
[vr],
rrans,trans-alka-2,4- dienal).
THERMALLY-STRESSED CULINARY OILS
Pro-inflammatory Properties
The oxygen radical-mediated peroxidation
of
polyunsaturates in the knee-
joint of patients with inflammatory joint diseases (e.g., rheumatoid arthritis)
have been investigated in some detail, and elevated levels
of
lipid oxidation
products have been measured in inflammatory knee-joint synovial fluid,
an
apparent consequence of a cascade
of
radical reactions induced by localized
46
M.
GROOTVELD
ETA.
episodes of ‘oxidative stress’ in vivo. In view of their aggressive reactivity
toward many essential biomolecules, aldehydic lipid oxidation products exert
powerful pro-inflammatory actions, and Benedetti
er
al.
(1980) found that
injection of a mixture of peroxidized PUFA-derived carbonyl compounds
(predominantly
4-hydroxy-trans-2-nonenal
at a concentration of only 0.15
pM)
induced a significant inflammatory response (i.e. edema) in the hind paw of rats.
Intriguingly, Selley
ef
al.
(1992) used gas chromatography coupled with
mass
spectrometric detection to determine levels of
4-hydroxy-trans-2-nonenal
in blood plasma of patients with rheumatoid and osteoarthritis, and found that
although concentrations of this terminal peroxidation product in the osteoarthrit-
ics’ biofluids were similar to those of healthy vqlunteers (ca. 0.10
pM),
those
of rheumatoid patients’ plasma were significantly greater. Although at least some
of this cytotoxic agent could arise from the oxidative degradation of PUFAs in
vivo, there may be an association between these levels and the frequency of
thermally-stressed PUFA consumption in the diet.
Several of the authors have recently investigated the pro-inflammatory
properties of control and thermally-stressed culinary oils using an appropriate
animal model system (foot pad edema in the hind paw of male Wistar albino
rats), and Fig. 2 demonstrates that preheating corn and olive oils at a tempera-
ture of 250C for a period of 60 min gives rise to a marked elevation in the pro-
inflammatory properties of these materials. The increase in edema size with time
observed for the heated
corn
oil samples is significantly greater than that arising
from heated olive oil samples, a phenomenon explicable by the much higher
content of PUFAs in the former which, of course, give rise to the generation
of
higher concentrations
of
aldehydic peroxidation products.
Gastropathic
Conditions
Oral administration of the a$-unsaturated aldehyde 4-hydroxy-rrans-2-
nonenal to rats at a dose level of only 0.26
pM,
a concentration similar to that
of healthy human blood plasma,
has
been found to induce peptic ulcers in the
animals (Jayaraj
er
al.
1986). Therefore, dietary consumption of such agents,
present at extremely high levels in thermally-stressed PUFA-rich culinary oils,
may account for a high fraction of such gastopathic conditions in humans.
In contrast to the acute toxicity observed shortly after the systemic
administration of CHPDs (experimental animals dying from severe lung damage
within 24 h), oral administration of these primary lipid oxidation products were
found to be nonlethal, a phenomenon indicating that they fail to be effectively
absorbed across the gastric or intestinal epithelium. However, it is important to
note that isomeric CHPDs could also give rise to gastropathic conditions in
humans consuming culinary oils subjected to domestic or commercial frying
episodes.
HEATED
OILS:
HEALTH EFFECTS
47
Mutagenicity
and
Genotoxicity
Further toxicological investigations regarding thermally-stressed culinary
oils and fats have focussed on their mutagenic properties. Indeed, recent studies
by Wu
ef
al.
(1999) and Zhong
ef
al.
(1999) have shown that volatile emissions
from heated culinary oils utilized for the purpose of Chinese-style cooking
are
mutagenic and exposure to such indoor air pollution may render humans to
an
increased risk of contracting lung cancer. Indeed, in view of the temperatures
employed in standard frying practices
(ca.
180C), such fumes are rich in
CHPD-derived volatile aldehydic fragments, including acrolein, one of the most
highly toxic crJ3-unsaturated aldehydes generated from the thermally-induced
oxidation of PUFAs.
Intriguingly, Shields
et
al.
(1995) found that volatile emissions from
unrefined Chinese rapeseed, refined U.S. rapeseed (Canola), Chinese soybean
and Chinese peanut oils contained the mutagens acrolein and formaldehyde in
addition to 1,3-butadiene and benzene, which represent important risk factors in
the etiology of lung cancer. As expected, lowering of the cooking temperature,
or pre-addition of lipid-soluble antioxidants such
as
butylated hydroxyanisole
(BHA) decreased the levels of these mutagenic volatile components, and,
interestingly, the mutagenicity of individual volatile emission condensates
correlated strongly with the linolenate content of the oils investigated.
Hence, the inhalation of vaporized aldehydes by subjects conducting
commercial or domestic frying practices involving PUFA-rich culinary oils
affords a potential hazard to human health.
The mutagenic properties of repeatedly-used deep-frying fats have been
previously evaluated using the Ames test (Hageman
et
al.
1988). In this study,
fat samples were fractionated into polar and nonpolar fractions by column
chromatography and the former increased the number of revertants without S-9
mix in various strains, strain TA97 being the most sensitive. The mutagenic
activity of these polar fractions was positively correlated with the level of
thiobarbituric acid-reactive substances (TBARS), an observation strongly
suggesting the involvement of lipid oxidation products in mutagenicity.
Teratogenicity
The possibility that heated culinary oils might stimulate the development of
birth defects has been studied only recently.
Two
of the contributors of this
paper, B. Serra and
M.
Viana, have obtained evidence indicating that both
in
vifro
and
in vivo,
the generation
of
oxygen-derived free radical species can lead
to embryo malformations (Bonet
ef
al.
1995; Viana
ef
al.
1996). These findings
are consistent with reports from other laboratories on the embryonic malforma-
tions due to oxygen-derived free radicals induced by diabetes (Eriksson and Borg
48
M.
GROOTVELD
ETA.
I
I
1991; Sivan
er
al.
1996) and the ameliorating effects
of
vitamin
E
(Bonet
ec
al.
1995;
Siman
and Eriksson 1997).
I
30
B
v
W
u
3
25
E
I2
u
ri
3
d
20
I
15
-
-0
O.lOmL
of
unheated
corn
oil
0.lOmL
of
heated
corn
oil
***
***
T
r
ns
i/
,’
cj
I
***
I
I
*
1
rn
ns
I
TIME
(hr.)
HEATED
OILS:
HEALTH EFFECTS
I
I
I
I
30
25
20
15
!I
0
0.lOmL
Of
UNHEATED olive oil
-m
O.lOrnL
of
HEATED olive oil
**
**
ns
*
r
I
I
T\
'\
+I
T
ns
ns
Xh
1-
ns
rn
I
0
1.0
2.0
3.0
4.0
5.0
6.0
'
24.0
TIME
(hr.)
FIG. 2. PRO-INFLAMMATORY PROPERTIES
OF
THERMALLY-STRESSED CULINARY
OILS
Rat (male Wistar) foot pad edema induced by application of
0.10
mL
volumes of (A) control
(unheated) and preheated corn oil and
(B)
control and preheated olive oil
(oils
were subjected to a
60
min thermal saessing episode at 250C and then cooled
to
ambient temperature prior
to
testing).
Paw circumferences were measured with a cotton loop
localized
at the hindmost spur on the
subplatar surface. Data
points
are the mean values of groups of
6
experimental animals, and the
error bars represent associated
standard
deviations. Abbreviations:
ns,
not significantly significant;
*, **,
***,
statistically significant at the
5,
1
and
0.10%
levels, respectively.
50
M. GROOTVELD
ETA.
The mechanisms of these teratogenic effects are the subject of much
speculation. Among the cell components, PUFAs are readily oxidized by free
radicals, leading to the generation of cytotoxic aldehydic fragments (Gutteridge
and Halliwell
1994;
Pryor
1994).
These compounds can cause chromosomal
breakage (Emerit
ef
al.
1985;
Emerit
1994),
and if
this
process occurs in the
embryo,
it
could lead to malformations.
To
study whether culinary oils oxidized
by heat, materials rich in CHPDs and aldehydes, are teratogenic in rats, we
developed the following experiment (Bonet
et al.
1996).
Pregnant rats were fed
by gavage with
0.3
mL
of either thermally-stressed (with a content of TBARS
of
120
mmol) or nonheated sunflower
seed
oils from day
1
of pregnancy until
day
11,
the end of the rat gestational period.
A
control group was investigated.
The animals were sacrificed and the embryos examined.
In
Table
1,
the rate of
neural tube malformations, reabsorptions, crown-rump length and the number
of somites (parameters related with the embryo size and development) in the
three experimental groups are shown. Clearly, the administration of preheated
(oxidized) oil increased the mean rate of malformations from the
6%
found in
controls animals to a value of
26%.
The administration of nonheated oil did not
give rise to any changes in the rate of fetal malformations (the administration of
either preheated or nonheated culinary oil did not lead to any modifications
in
the rate
of
reabsorptions, crown-rump length, or the somite number). These
results demonstrate that the administration of aldehyde-containing thermally-
stressed culinary oil is highly teratogenic in the rat, and an attractive hypothesis
is that the intake of such oxidized oils during pregnancy may be partially
responsible for the neural tube defects found in humans. Differences in the type
of heated oil used in standard frying or cooking processes may also be
responsible for the differing rates of neural tube defects found among different
populations. Further investigations are required in this research area.
TABLE
1.
AND SOMITE NUMBER IN THE DIFFERENT EXPERIMENTAL GROUPS
RATE OF EMBRYO MALFORMATIONS, REABSORPTIONS, CROWN-RUMP LENGTH
Unheated
oil
Control Heated oxidized oil
Total embryos
132 50 105
Neural tubes malformed,
%
4.6 6.0 26.0
Reabsorptions,
%
9.5 10.0 7.5
Somites. number
29.5ko.i 2a.6ko.2 2a.5+0.3
Crown-rump, mm
4.1+0.03 3.9k0.05 3.9+0.05
HEATED
OILS:
HEALTH EFFECTS
51
Suggested
Research Activities
Several areas of research could potentially be fruitful with regard to
building upon what is currently known about the chemical breakdown and
toxicity of heated polyunsaturated oils and other frying fats. These include
surveys of foods provided in fast food restaurants, studies of improved
maintenance of oils during restaurant usage by, for example, improved use of
antioxidants, improved filtration efficiency, determining the optimum
type
of oil
(fat) to use in a frying operation, and in some cases development of alternative
cooking procedures i.e. those which create food with fried characteristics but in
fact do not employ oils in the cooking process. In addition, although not
specifically reviewed in this article, precooked (uncured) meats and irradiated
meats are two types of food that may well contain lipid oxidation products
similar to those in heated polyunsaturated oils and therefore parallel studies
should be conducted.
Surveys of foods are needed to ascertain the actual consumption of lipid
oxidation products by the public. Given the complexities involved, i.e. the many
different types of fats, oils and shortenings; the many types of maintenance
schedules and equipment; the numerous foods, extremely variable in composition
and properties, that are fried, such a survey would be a major undertaking but
it must be conducted. It would also be valuable to compare restaurants that are
subjected to governmental regulation regarding oil quality, specifically regulating
maximum polar materials allowable, and those that are not. Methodology used
to monitor oil quality is also an important issue. One way to insure minimum
acceptable oil quality would be to incorporate the oil quality requirements and
maintenance schedule into the restaurant's HACCP (hazard analysis critical
control point) program. The implementation of a HACCP program for frying
oils would require the development of effective quality control (rapid, simple)
tests for oil quality.
REFERENCES
ADDIS, P.B.
1986.
Occurrence of lipid oxidation products in foods. Food
Chem. Toxicol.
24,
1021-1030.
ADDIS, P.B., CARR, T.P, HASSEL, C.A., HUANG,
Z.Z.
and WARNER,
G.
J.
1995.
Atherogenic and anti-atherogenic factors in the human diet.
Biochem. SOC. Symp.
61,
259-271.
ADDIS, P.B., EMANUEL, H.A., BERGMANN, S.D. and ZAVORAL, J.H.
1989.
Capillary GC quantification of cholesterol oxidation products in
plasma lipoproteins of fasted humans. Free Radical Biol. Med.
7,179-182.
52
M.
GROOTVELD
ETA.
ADDIS, P.B. and WARNER, G.J.
1991.
The potential health aspects of lipid
oxidation products in food. In
Free Radicals and Food Additives,
(0.1.
Arouma and B. Halliwell, eds.) pp.
77-119,
Taylor and Francis Ltd.,
London.
ADDIS, P.B., WARNER, G.J. and HASSEL, C.A.
1993.
Dietary lipid
oxidation products: are they atherogenic? Can.
J.
Cardiol.
9,
6B-10B.
BENEDE'ITI, A., FERRALI, M., CASINI, A.F., PEIRI,
S.
and COMPORTI,
M.
1990.
Foot edema induced by carbonyl compounds originating from the
peroxidation of liver microsomal lipids. Biochemical Pharmacol.
29,
BONET,
B.,
VIANA, M. and HERRERA, E.
1995.
Teratogenic effects of
Diabetes: Protection by vitamin E.
2nd
International Symposium on
Diabetes and Pregnancy in the
90's.
Jerusalem, Israel.
BONET, B., VIANA, M., LAGOS, D. and SOTILLO, R.
1996.
Teratogenic
effects of oxidized oil. VIII Biennial Meeting, International Society for
Free Radical Research. Barcelona, Spain.
CLAXSON, A.W.D., HAWKES, G.E., RICHARDSON, D.P., NAUGHTON,
D.P., HAYWOOD, R.M., CHANDER, C.L., ATHERTON, M.,
LYNCH, E.J. and GROOTVELD, M.C.
1994.
Generation of lipid
peroxidation products in culinary oils and fats during episodes of thermal
stressing: a high field 'H NMR study. FEBS Lett.
355,
81-90.
EMANUEL, H.A., HASSEL, C.A., ADDIS, P.B., BERGMANN, S.P. and
ZAVORAL, J.H.
1991.
Plasma cholesterol oxidation products (oxysterols)
in human subjects fed a meal rich in oxysterols. J. Food Sci.
56,
843-847.
EMERIT,
I.,
KECK, M., LEVY, A., FEINGOLD, J. and MICHELSON,
A.M.
1985.
Activated oxygen species at the origin of chromosome
breakage and sister chromatid exchanges. Mutation Res.
103,
165-172.
EMERIT, I.
1994.
Reactive oxygen species, chromosome mutation, and cancer:
possible role of clastogenic factors in carcinogenesis. Free Radical Biol.
&
Medicine
16,
99-109.
ERIKSSON,
U.J.
and BORG, L.A.H.
1991.
Diabetes and embryonic malforma-
tions: role of substrate-induced free-oxygen radical production for
dysmophogenesis in cultured rat embryos. Diabetes
42,
41 1-419.
ESTERBAUER, H.
1982.
Aldehydic products of lipid peroxidation. In
Free
Radicals, Lipid Peroxidation and Cancer,
(D.C.H. McBrien and T.F.
Slater, eds.) pp.
101-128,
Academic Press, London.
GROOTVELD, M., ATHERTON, M.D., SHEERIN, A.N., HAWKKES, J.,
BLAKE, D., RICHERNS, T.E., SILWOOD, C.J.L., LYNCH, E. and
CLAXSON, A.W.D.
1998.
In
vivo
absorption, metabolism and urinary
excretion of cr,&unsaturated aldehydes in experimental animals: Relevance
to the development of cardiovascular diseases by
the
dietary ingestion of
12 1- 124.
HEATED
OILS:
HEALTH EFFECTS
53
thermally-stressed polyunsaturate-rich culinary oils. J. Clin. Invest.
101,
GUARDIOLA, F., CODONY, R., ADDIS, P.B., RAFECAS, M. and
BOATELLA, J.
1996.
Biological effects of oxysterols: current status. Food
Chemical Toxicol.
34,
193-211.
GUTTERIDGE, J.M.C. and HALLIWELL, B.
1994.
Antioxidants in Nutrition,
Health
and
Disease.
Oxford University Press, New York.
HAGEMAN, G., HERMANS, R., TEN HOOR,
F.
and KLEINJANS, J.
1988.
Assessment of mutagenic activity of repeatedly used deep-frying fats.
Mutation Res.
204,
593-604.
HAYES, K.C.
1996.
Designing a cholesterol-removed fat blend for frying and
baking. Food Technol.
50(4), 92-97.
HAYWOOD, R.M., CLAXSON, A. W.D., HAWKES, G.E., RICHARDSON,
D.P., COUMBARIDES, G., HAWKES, J., LYNCH, E.J. and
GROOTVELD, M.C.
1995.
Detection of aldehydes and their conjugated
hydroperoxydiene precursors in thermally-stressed culinary oils and fats:
investigations using high resolution proton NMR spectroscopy. Free Rad.
Res.
22,
441-482.
HASSEL, C.A., WARNER, G.J., JIA, X. and ADDIS, P.B.
1992.
The
metabolic fate of certain cholesterol oxides in studies on hamsters. Inform.
3,
525.
HOFF, H.F., O’NEIL, J., CHISOLM, G.M., COLE, T.B.,
QUEHENBERGER, D., ESTERBAUER, H. and JURGENS, G.
1989.
Modification of low-density lipoprotein with 4-hydroxynonenal induces
uptake by macrophages. Arteriosclerosis
9,
539-549.
JAYARAJ, A.P., REES, K.R., TOVEY, F.E. and WHITE,
J.S.
1986.
A
molecular basis of peptic ulceration due to diet. Brit. J. Exp. Pathol.
67,
JOHNSON, M.H., ADDIS, P.B. and EPLEY, R.J.
1994.
Rancidity in beef
patties and reduction by wild rice. J. Foodservice Systems
8,
47-59.
JURGENS, G., HOFF, H.F., CHISOLM
111,
G.M. and ESTERBAUER, H.
1987.
Modification of human serum low density lipoprotein by oxidation:
characterization and pathophysiological implications. Chem. Phys. Lipids
KRITCHEVSKY, D. and TEPPER, S.A.
1967.
Cholesterol vehicle in
experimental atherosclerosis.
9.
Comparison of heated corn oil and heated
olive oil. J. Atheroscler. Res.
7,
647-651.
PARK, S.W. and ADDIS, P.B.
1985.
Capillary column gas-liquid chromato-
graphic resolution of oxidized cholesterol derivatives. Anal. Biochem.
149,
12 10- 12 18.
149- 155.
45,
315-316.
275-283.
54
M.
GROOTVELD
ETA.
PARK, S.W. and ADDIS, P.B. 1986a. Identification and quantitative estimation
of oxidized cholesterol derivatives in heated tallow. J
.
Agric. Food Chem.
PARK, S.W. and ADDIS, P.B. 1986b. Further investigation of oxidized
cholesterol derivatives in heated fats. J. Food Sci.
5,
1380-1381.
PARK, S.W. and ADDIS, P.B. 1987. Cholesterol oxidation products in some
muscle foods. J. Food Sci.
52,
1500-1503.
PARK, P.S.W. and ADDIS, P.B. 1989. Derivatization of Sa-cholestane-
38,5,6@-triol into trimethyl ether sterol for
GC
analysis. J. Amer. Oil
Chem. SOC.
66,
1632-1634.
PARK, P.W., GUARDIOLA, F. and ADDIS, P.B. 1996. Kinetic evaluation of
3~-hydroxycholest-5-en-7-one
(7-ketocholesterol) stability during saponifi-
cation. J. Amer. Oil Chem.
SOC.
73,
623-629.
PRYOR, W.A. 1994. Free radicals and lipid peroxidation: what they are and
how they got that way. In
Natural Antioxidants in
Human
Health and
Disease.
(B.
Frei, ed.) pp. 1-24, Academic Press, London.
SANDER, B.D., SMITH, D.E. and ADDIS, P.B.
1988.
Effects of processing
and storage conditions on levels of cholesterol oxidation products in butter
and Cheddar cheese. J. Dairy Sci.
71,
3173-3178.
SELLEY, M.L., BOURNE, D.J., BARTLET", M.R., TYMMS, K.E.,
BROOK, A.S., DUFFIELD, A.M. and COMFQRTI, M. 1992. Occur-
rence of (E)-4-hydroxy-2-nonenal in plasma and synovial fluid of patients
with rheumatoid and osteoarthritis. Ann. Rheum. Dis.
51,
481-484.
SHIELDS, P.G., XU, G.X., BLOT, W.J., FRAUMENI JR., J.F., TRIVERS,
G.E., PELLIZARI, E.D., QU, Y.H., GAO, Y.T. and HARRIS, C.C.
1995. Mutagens from heated Chinese and US cooking oils. J. National
Cancer Inst.
87,
836-841.
SIMAN, C.M. and ERIKSSON, U.J. 1997. Vitamin E decreases the occurrence
of malformations in the offspring of diabetic rats. Diabetes
46,
1054-1061.
SIVAN, E., REECE, E.A., WU, Y.K., HOMKO, C.J., POLANSKY, M. and
BORENSTEIN, M. 1996. Dietary vitamin E prophylaxis and diabetic
embryopath: morphological and biochemical analysis.
Am.
J.
Obstet.
Gynecol.
175,
793-799.
SMITH, T. and KUMMEROW, F.A. 1987. In
Nutrition
and
Heart Disease,
Vol. 1, (R.R. Watson, ed.) pp. 45-64, CRC Press, Boca Raton, Florida.
STAPRANS,
I.,
RAPP, J.H., PAN, X.M., HARDMAN, D.A. and
FEINGOLD, K.R. 1996. Oxidized lipids in the diet accelerate the
development of fatty streaks in cholesterol-fed rabbits. Arterioscler.
Thromb. Vasc. Biol.
16,
533-538.
STEINBERG, D. and WITZTUM, J.L. 1990. Lipoproteins and atherogenesis:
current concepts. J. Amer. Med. Assoc.
246,
3047-3052.
34,
653-659.
HEATED
OILS:
HEALTH EFFECTS
55
SUNDRAM, K., ISMAIL, A. and HAYES, K.C. 1997.
Trans
(elaidic) fatty
acids adversely affect the lipoprotein profile relative to specific saturated
fatty acids in humans. J. Nutrition
127,
514s-520s.
VAN HINSBERGH, V.W.H. 1984. LDL cytotoxicity. The state of the
art.
Atherosclerosis
53,
113-1 18.
VIANA, M., HERRERA, E. and BONET,
B.
1996. Teratogenic effects of
diabetes: Prevention by vitamin E. Diabetologia
39,
1041-1046.
WU, P.F., CHIANG, T.A., KO, Y.C. and LEE, H. 1999. Genotoxicity of
fumes from heated cooking oils produced
in
Taiwan. Environ. Res.
80,
ZHANG, W.B. and ADDIS, P.B. 1990. Prediction of levels of cholesterol
oxides in heated tallow by dielectric measurement.
J.
Food Sci.
55,
ZHANG, W.B. and ADDIS, P.B. 1991. Quantification of 5a-cholestane-
30,5,6a-triol and other cholesterol oxidation products in fast food French
fries. J. Food Sci.
56,
716-718.
ZHANG, W.B. and ADDIS, P.B. 1992. Evaluation of frying oil filtration
systems. J. Food Sci.
57,
651-654.
ZHONG,
L.,
GOLDBERG, M.S., PARENT, M.E. and HANLEY, J.A. 1999.
Risk
of
developing lung cancer in relation to exposure to fumes from
Chinese-style cooking. Scandinavian J. Work Environ. Health
25,
122- 126.
1673-1675.
309-316.
... The assignment of the resonances of both primary and secondary LOPs identified in the 1 H NMR spectra of the thermally stressed culinary oils were performed according to [3,6,12,[16][17][18][19][20][21]. Amongst all the LOPs identified and characterized, only secondary or tertiary aldehydic LOPs were quantified. ...
... In general, the concentration magnitudes of these secondary LOPs were found to be in the order walnut > corn > sesame > groundnut > extra virgin olive > macadamia oils > ghee (Figure 3ii). Aldehydic LOPs identified in this report are fully consistent with those reported by [5,6,8,[16][17][18]20,21,33,34]. ...
Article
Full-text available
Scientific warnings on the deleterious health effects exerted by dietary lipid oxidation products (LOPs) present in thermally stressed culinary oils have, to date, not received adequate attention given that there has been an increase in the use and consumption of such oil products in everyday life. In this study, high-resolution 1H nuclear magnetic resonance (NMR) analysis was used to characterize and map chemical modifications to fatty acid (FA) acyl groups and the evolution of LOPs in saturated fatty acid (SFA)-rich ghee, monounsaturated fatty acid (MUFA)-rich groundnut, extra virgin olive, and macadamia oils, along with polyunsaturated fatty acid (PUFA)-rich sesame, corn and walnut oils, which were all thermally stressed at 180 °C, continuously and discontinuously for 300 and 480 min, respectively. Results acquired revealed that PUFA-rich culinary oils were more susceptible to thermo-oxidative stress than the others tested, as expected. However, ghee and macadamia oil both generated only low levels of toxic LOPs, and these results demonstrated a striking similarity. Furthermore, at the 120 min thermo-oxidation time-point, the discontinuous thermo-oxidation episodes produced higher concentrations of aldehydic LOPs than those produced during continuous thermo-oxidation sessions for the same duration. On completion of the thermo-oxidation period, a higher level of triacylglycerol chain degradation, and hence, higher concentrations of aldehydes, were registered in culinary oils thermally stressed continuously over those found in discontinuous thermo-oxidized oils. These findings may be crucial in setting targets and developing scientific methods for the suppression of LOPs in thermo-oxidized oils.
... Globally, the recommendation of health and nutrition authorities that such culinary frying oils (CFOs) are the most 'healthfriendly' prerogatives available for food frying applications may present a challenging issue, since these now directly conflict with a plethora of scientific results acquired by many research groups globally. Indeed, for many of the valuable population health properties potentially offered by pure unmodified, uncontaminated and unoxidized dietary PUFAcontaining acylglycerols, the converse is the case for dietary LOPs, especially aldehydes and epoxy-FAs derived from the peroxidation of unsaturated fatty acids (UFAs) [9][10][11]; very high levels of these toxins are generated during the exposure of UFA-rich (most especially PUFA-rich) edible oils to high temperature frying practices [12,13]. ...
... In view of these considerations, such secondary LOPs give rise to a broad spectrum of concentration-dependent cellular stresses. The deleterious toxicological properties and health effects of these aldehydes represent one major consequential focus of this communication, and these include their adverse influence on critical metabolic pathways (for example, [26]); promotion and perpetuation of atherosclerosis and cardiovascular diseases [23,[27][28][29]); mutagenic and carcinogenic properties [30][31][32][33][34][35]; teratogenic actions (embryo malformations during pregnancy [36]; exertion of striking pro-inflammatory effects [10,37]; induction of gastropathic properties (peptic ulcers) following dietary ingestion [38]; neurotoxic actions, including those of 4-hydroxy-trans-2-nonenal (HNE) and -hexenal (HHE) [39]; and the adverse stimulation of significant increases in systolic blood pressure [40]. Further deleterious health effects include chromosomal aberrations, reflecting their clastogenic potential, and sister chromatid exchanges and point mutations, in addition to cell damage and death [41,42]. ...
Article
Full-text available
Continuous or frequent ingestion of fried foods containing cytotoxic/mutagenic/genotoxic lipid oxidation products (LOPs) may present significant human health risks; such toxins are generated in thermally stressed polyunsaturated fatty acid (PUFA)-rich culinary frying oils (CFOs) during standard frying practices. Since monounsaturated and saturated fatty acids (MUFAs and SFAs, respectively) are much less susceptible to peroxidation than PUFAs, in this study CFOs of differential unsaturated fatty acid contents were exposed to laboratory-simulated shallow-frying episodes (LSSFEs). Firstly, we present a case study exploring the time-dependent generation of aldehydic LOPs in CFO products undergoing LSSFEs, which was then used to evaluate the relative potential health risks posed by them, and also to provide suitable recommendations concerning their safety when used for frying purposes. Sunflower, rapeseed, extra-virgin olive and coconut oils underwent LSSFEs at 180 °C: Samples were collected at 0–90 min time-points (n = 6 replicates per oil). Aldehydes therein were determined by high-resolution 1H NMR analysis at 400 and 600 MHz operating frequencies. For one of the first times, CFO LOP analysis was also performed on a non-stationary 60 MHz benchtop NMR spectrometer. 1H NMR analysis confirmed the thermally promoted, time-dependent production of a wide range of aldehydic LOPs in CFOs. As expected, the highest levels of these toxins were produced in PUFA-rich sunflower oil, with lower concentrations formed in MUFA-rich canola and extra-virgin olive oils; in view of its very high SFA content, only very low levels of selected aldehyde classes were generated in coconut oil during LSSFEs. Secondly, 1H NMR results acquired are discussed with regard to the suitability and validity of alternative, albeit routinely employed, spectrophotometric methods for evaluating the peroxidation status of CFOs and lipid-containing foods. Thirdly, an updated mini-review of the toxicological properties of and intake limits for LOPs, and deleterious health effects posed by their ingestion, is provided. In conclusion, exposure of PUFA-rich CFOs to high-temperature frying practices generates very high concentrations of aldehydic LOP toxins from thermally promoted, O2-powered, recycling peroxidation processes; these toxins penetrate into and hence are ‘carried’ by fried foods available for human consumption. Such toxins have the capacity to contribute towards the development and progression of non-communicable chronic diseases (NCDs) if cumulatively ingested by humans.
... Moreover, a similar volume of reports which associate increased risks of NCDs such as selected cancers and cardiovascular diseases with an excessive dietary consumption of fried foods, are also readily accessible. Indeed, aldehydic LOPs bolster a very wide range of deleterious, concentrationdependent health effects, and an inexhaustive summary of these includes the induction and proliferation of atherosclerosis and its cardiovascular disease sequelae (12)(13)(14); mutagenic and carcinogenic effects (15,16); neurotoxic properties, particularly for formaldehyde, acetaldehyde, and 4-hydroxy-trans-2-nonenal (HNE) and -hexenal (HHE) (17); the exertion of astonishing pro-inflammatory effects at very low concentrations (18,19); very concerning teratogenic actions (20); and gastropathic properties (peptic ulcers) subsequent to their dietary intake (21). These reports clearly provide powerful evidence for potential public health threats induced and perpetuated by LOPs present as food-borne toxins. ...
Article
Full-text available
In this manuscript, a series of research reports focused on dietary lipid oxidation products (LOPs), their toxicities and adverse health effects are critically reviewed in order to present a challenge to the mindset supporting, or strongly supporting, the notion that polyunsaturated fatty acid-laden frying oils are “safe” to use for high-temperature frying practises. The generation, physiological fates, and toxicities of less commonly known or documented LOPs, such as epoxy-fatty acids, are also considered. Primarily, an introduction to the sequential autocatalytic peroxidative degradation of unsaturated fatty acids (UFAs) occurring during frying episodes is described, as are the potential adverse health effects posed by the dietary consumption of aldehydic and other LOP toxins formed. In continuance, statistics on the dietary consumption of fried foods by humans are reviewed, with a special consideration of French fries. Subsequently, estimates of human dietary aldehyde intake are critically explored, which unfortunately are limited to acrolein and other lower homologues such as acetaldehyde and formaldehyde. However, a full update on estimates of quantities derived from fried food sources is provided here. Further items reviewed include the biochemical reactivities, metabolism and volatilities of aldehydic LOPs (the latter of which is of critical importance regarding the adverse health effects mediated by the inhalation of cooking/frying oil fumes); their toxicological actions, including sections focussed on governmental health authority tolerable daily intakes, delivery methods and routes employed for assessing such effects in animal model systems, along with problems encountered with the Cramer classification of such toxins. The mutagenicities, genotoxicities, and carcinogenic potential of aldehydes are then reviewed in some detail, and following this the physiological concentrations of aldehydes and their likely dietary sources are considered. Finally, conclusions from this study are drawn, with special reference to requirements for (1) the establishment of tolerable daily intake (TDI) values for a much wider range of aldehydic LOPs, and (2) the performance of future nutritional and epidemiological trials to explore associations between their dietary intake and the incidence and severity of non-communicable chronic diseases (NCDs).
... Aldehydic LOPs have been identified and characterized in several oil types, and these include culinary oils of varying degree of unsaturation (Claxson et al., 1994;Haywood et al., 1995;Grootveld et al., 2001;Guillén & Uriarte, 2009;Goicoechea & Guillén, 2010;Grootveld et al., 2014;Castejón et al., 2017;Le Gresley et al., 2019a;Ampem et al., 2021), margarines (Ibargoitia et al., 2014), cod liver oils (Percival et al., 2020b), monounsaturated-rich algae oil (Moumtaz et al., 2019), extracts of French fries (Silwood & Grootveld, 1999;Grootveld et al., 2014;Grootveld et al., 2018;Le Gresley et al., 2019a;Le Gresley et al., 2021), as well as crude and processed pyrolysis oil (Le Gresley et al., 2019b). ...
Article
Full-text available
Suppressing toxic aldehydic lipid oxidation product (LOP) generation in culinary oils is now considered vital, since the deleterious effects arising from their ingestion are implicated in a wide range of disease conditions. Partial substitution involves the replenishment of thermally-stressed culinary oils with corresponding unheated ones. This technique was tested by employing 10%, 25%, 50%, and 75% (v/v) partial substitutions of coconut, olive, rapeseed, and sunflower oils at 180℃ for a 300 min continuous thermo-oxidation duration. Oil samples were analysed by proton nuclear magnetic resonance (¹H NMR) spectroscopy. Trace metal levels, including oxidation-reduction (redox)-active metal ions credited with enhancing cooking oil oxidation were also analysed using inductively coupled plasma-optical emission spectroscopy (ICP-OES). As expected, the degree of oil unsaturation, and the % partial substitutions significantly influenced their susceptibility to thermo-oxidation. In view of the very low polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) contents of coconut oil, both the class and concentrations of evolved LOPs were found to be least affected by this partial substitution process. Aldehydic LOPs were greatly suppressed in partially-substituted rapeseed oil. The % suppression activity of LOPs evaluated for the partially substituted oils were generally high making partial oil substitutions an effective chemical-free method in suppressing LOPs at both industrial and commercial levels. In general, the % partial oil substitutions were directly related to the dilution effect observed for LOPs quantified in the oils. Furthermore, trace metal ion concentrations measured in the culinary oils did not influence the evolution of LOPs in the oils.
... Perhaps the most dramatic toxicity findings of LOPs in heated oils was the teratogenic effects reported by Bonet and colleagues of Madrid, Spain [20], a development also reviewed by Grootveld et al. [21], in a journal serving the foodservice industry. The teratogenic effects noted translate to neural tube defects such as spina bifida. ...
... LOPs formed from this thermally-induced peroxidation of frying oil unsaturated fatty acids (UFAs) have been shown to exert both mutagenic and carcinogenic properties (1,2). They also have potent proinflammatory actions (3,4), increase systolic blood pressure (5), and can also induce cell damage and death through the induction of chromosomal abberations (6, 7). ...
Article
Full-text available
Differences in lipid oxidation products (LOPs) and trace metal concentrations of French fry samples found between two global chain fast-food restaurants in the UK were investigated using high-resolution proton nuclear magnetic resonance ( ¹ H NMR) and inductively coupled plasma-optical emission spectrometry (ICP-OES) analyses, respectively, of extracts derived therefrom. Over the course of 3 days and 3 different diurnal time periods, samples of French fries (FFs) were analyzed, and comparisons of two different oil extraction methods were undertaken for the two restaurants involved. The magnitude of concentrations of LOPs extracted from FFs is discussed. Significant differences between 6/7 aldehyde classifications, and aluminum, manganese, vanadium, lead, iron, copper and nickel levels between samples from the two restaurants are also reported. Redox-active transition and further trace metal concentrations inversely correlated with FF oil sample LOP contents; this suggested an antioxidant rather than a pro-oxidant role for them.
Article
Full-text available
Suppressing the evolution of lipid oxidation products (LOPs) in commercially available culinary oils is considered to represent a valuable health-promoting incentive since these agents have cytotoxic and genotoxic properties and have been implicated in the pathogenesis of several chronic disease states. One agent used to suppress LOPs formation is polydimethylsiloxane (PDMS). In this study, proton nuclear magnetic resonance ( ¹ H NMR) analysis was employed to evaluating the influence of increasing PDMS concentrations (6.25 × 10 ⁻⁷ , 1.0 × 10 ⁻⁵ , 0.025, 0.05, 0.1, 0.5, 1.0, 5.0, and 10.0 ppm) in either stirred or unstirred refined sunflower oil exposed to thermal stressing episodes continuously at 180°C for 300 min with no oil replenishment. Results acquired showed that the extent of blockage of LOPs generation was correlated with increasing concentrations of PDMS. The minimal level of added PDMS required to provide a statistically significant protective role for both stirred and unstirred culinary oils when exposed to high frying temperatures was only 6.25 × 10 ⁻⁷ ppm. Furthermore, stirring at 250 rpm was experimentally determined to reduce the functional role PDMS. This is vital in a real world setting since the boiling process of frying may ultimately reduce the LOPs suppression activity of PDMS.
Article
Full-text available
Oils are usually used for cooking purposes and claimed to protect against many disease like coronary heart disease, hypercholesterolemia, obesity, cancers and hypertension. This study was carried out to evaluate the effect of fresh and repeatedly-boiled peanut and olive oils (boiled five times) on blood lipid profile (High density lipoprotein HDL, low density lipoprotein LDL, Triglyceride TG and cholesterol) and their effect on weight and hematological parameters. Thirty Wistar rats were divided to five groups, control, fresh olive oil, boiled olive oil, fresh peanut oil, boiled peanut oil; in doses of 1 mg/kg/day plus cholesterol in 2 mg/kg/day being dissolved in bile and diluted 50% in distilled water, given orally for three weeks except control group which did not received neither cholesterol nor oil. All groups of rats showed decreased body weight when compared to the controls. Significant changes on WBCs, lymphocytes and neutrophils were also observed. On the other hand, lipid profile analysis showed significant increase (p<0.05) in serum cholesterol of fresh oils fed groups of rats, but significantly decreased in repeatedly-boiled oils. Significant increase (p<0.05) of triglycerides was observed in fresh oils fed groups where as no change was seen in stressed oil fed groups. Higher values of HDL were shown in fresh oils fed groups but no change was seen in repeatedly-boiled groups. Significant decrease of LDL was observed in all test groups when compared to the controls.
Article
Full-text available
Cooking oils are widely used in food preparation. During cooking, harmful compounds are formed in oils, therefore utilization of used cooking oils (waste cooking oils) is limited. Single cell protein (SCP) is dietary protein, which can be produced from various protein-rich microorganisms that are capable of utilizing industrial by-products such as waste cooking oil (WCO). In this study the utilization of industrial WCO (obtained from local potato chips manufacturer) as a carbon source for single cell protein production by yeast Yarrowia lipolytica was assessed. The medium containing 27.5 g/L WCO and C/N ratio of 5–10 for batch fermentations was determined to be the optimal composition for SCP production. In this study, the highest reported Yarrowia lipolytica biomass concentration (57.37 g/L) was achieved when WCO was used as the main carbon source. Protein concentrations were relatively low (12.6 %), which also affected the final protein yield (7.23 g/L). The resulting biomass accumulated low concentrations of toxic malondialdehyde (MDA) (2.32 mg MDA/kg) compared to concentrations initially detected in the WCO itself (30.87 mg MDA/kg). To the best of the authors knowledge this is the first study to report on MDA decrease via microbial fermentations.
Article
Saturated fat, modified to contain increased polyunsaturates and no cholesterol, provides desirable fat characteristics with positive effects on plasma lipoproteins.
Article
Chemical identity of 5α-cholestane-3β,5,6β-triol (C-Triol) as a trimethylsilyl (TMS) ether derivative was studied using gas chromatography (GC), mass spectrometry (MS), and proton nuclear magnetic resonance (NMR) spectroscopy. The derivatization mixture, held at 23°C for 30 and 300 min, showed only a single peak (B) by GC. When the mixture was heated at 70°C for a few hours, another peak (A) emerged ahead of peak (B). GC-MS analysis revealed that the GC peaks (A) and (B) are C-Triol astris- andbis-TMS ether derivatives, respectively. NMR analysis suggested that the hydroxyl groups at C3 and C6 of C-Triol were involved in the formation of thebis-TMS ether.
Article
Capillary gas chromatography was utilized to determine the amounts of cholesterol oxidation products in butter and Cheddar cheese. Butter was analyzed for COPS at five stages of processing, and there was little or no effect due to the processing conditions. Cholesterol oxidation products that did occur originated with the raw material. Storage of butter for up to 6 mo had little effect on cholesterol oxidation. Cheddar cheese was analyzed at various stages of processing. Again, there was little effect due to processing, and cholesterol oxidation products originated with the raw material. The ripening process did not result in any appreciable increase in cholesterol oxidation products.
Article
Oxidized cholesterol derivatives (OCDs) in tallow were isolated by saponification overnight at room temperature and quantified by a newly developed capillary gas chromatography method that includes trimethylsilylation. 7-Ketocholesterol and cholesterol α-epoxide added to tallow survived saponification as well as the other OCDs tested, displaying recoveries of at least 95%. Continuous heating of tallow at 155°C resulted in the formation of at least four OCDs as detected by capillary GC. OCDs were identified by capillary GC-mass spectrometry as 7α-hydroxy-, 7β-hydroxy-, and 7-ketocholesterol and α-epoxide. 7-Ketocholesterol was the predominant species formed. Its net formation was proportional to heating time, reaching up to ca. 10% of the initial content of cholesterol (in unheated tallow) after 376 h of heating. Capillary GC-MS also revealed the apparent formation of cholesterol β-epoxide in heated tallow.
Article
Three heated oil filtration systems were evaluated: (1) paper filter; (2) paper filter plus diatomaceous earth (DE); and (3) depth filtration with a filter pad under positive pressure. Methods 1 and 2 are traditional methods. Results on tallow-cottonseed oil (90:10) and hydrogenated soybean shortening indicated that depth filtration was more effective at maintaining lipid oxidation products at low levels than methods 1 and 2. Levels of free fatty acids did not appear to differ markedly between treatments in both comparisons of depth filtration with traditional methods. Mineral analysis of both heated oil filtrate and residue removed from oil by filters revealed that depth filtration was more effective at removal of pro-oxidant transition metals than were methods 1 and 2.
Article
The oxidation of cholesterol in tallow heated at various frying temperatures, 135°, 150°, 165°, and 180°C was studied by capillary gas chromatography. The linearity of formation of 7-ketocholesterol with heating time was confirmed. However, no significant differences in rate of formation of 7-ketocholesterol were noted among temperatures of 135°, 150°, and 165°C. Therefore, it was not possible to construct a kinetic equation. The possible efficacy of antioxidants at frying temperatures was demonstrated by incorporating ascorbyl palmitate plus dl-α-tocopherol into tallow at 135°C.
Article
Although rancidity is a well-documented quality problem in meat products, we are unaware of any comprehensive assessment of the extent of the problem. Therefore, ground beef products (fresh-frozen and precooked-frozen from supermarkets; cooked from fast food chains and high schools) were purchased in the Minneapolis-St. Paul area and analyzed for thiobarbituric acid reactive substances (TBARS). The TBARS values showed considerable variation among establishments with some establishments' products showing seriously elevated TBARS values. Because our laboratory had hypothesized that wild rice contains an antioxidant, extra lean ground beef (10% fat) was compared with extra lean ground beef patties containing wild rice at different levels, forms, and hydrations. Wild rice added at 15% prevented decrease in consumer acceptability during frozen storage. Whole grain wild rice was a more effective antioxidant than ground wild rice. Hydration level of wild rice did not appear to affect consumer like/dislike. Under certain conditions, hydrated wild rice can be an effective antioxidant in extra lean ground beef.
Article
Cholesterol oxidation products were estimated in some meat products by capillary gas chromatography after trimethylsilylation. Peak identities were confirmed by mass spectrometry. Freeze-dried pork, stored in contact with air at 22°C for ca. 3 yr, revealed 7- and 7β-hydroxycholesterol, 7-ketocholesterol, - and β-epoxide and cholestane-triol. The total concentration of oxidation products reached almost half of the remaining cholesterol content with 7-ketocholesterol as the predominant species. Some oxidation products were noted at a few ppm levels in broiled beef steaks, but not in precooked beef products. As rancidity development advanced in comminuted and cooked meats during storage, the oxidation of cholesterol became apparent.