Pharmacological effects of green tea on the gastrointestinal system
Marcel W.L. Koo, Chi H. Cho*
Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, L2-55 Laboratory Block, 21 Sassoon Road, Hong Kong, PR China
Accepted 1 July 2004
Available online 6 August 2004
Green tea is rich in polyphenolic compounds, with catechins as its major component. Studies have shown that catechins possess diverse
pharmacological properties that include anti-oxidative, anti-inflammatory, anti-carcinogenic, anti-arteriosclerotic and anti-bacterial effects. In
the gastrointestinal tract, green tea was found to activate intracellular antioxidants, inhibit procarcinogen formation, suppress angiogenesis
and cancer cell proliferation. Studies on the preventive effect of green tea in esophageal cancer have produced inconsistent results; however,
inverse relationships of tea consumption with cancers of the stomach and colon have been widely reported. Green tea is effective to prevent
dental caries and reduce cholesterols and lipids absorption in the gastrointestinal tract, thus benefits subjects with cardiovascular disorders. As
tea catechins are well absorbed in the gastrointestinal tract and they interact synergistically in their disease-modifying actions, thus drinking
unfractionated green tea is the most simple and beneficial way to prevent gastrointestinal disorders.
D 2004 Elsevier B.V. All rights reserved.
Keywords: Green tea; Tea polyphenol; Catechin; (?)-Epigallocatechin gallate; Gastrointestinal tract
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Diverse actions of tea catechins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Mechanisms of action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Bioavailability of green tea. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Green tea and the aerodigestive sites. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Green tea and the stomach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Green tea and the intestine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Overall perspectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Green tea is prepared from the young shoots of tea plant
Camellia sinensis. They are rich in flavonoids, and in green
tea mostly polyphenolic compounds such as catechins. The
tea leaves are immediately heated with rolling after harvest
to inactivate the enzyme, polyphenol oxidase, which is
capable of oxidizing the tea catechins to oligomeric and
polymeric derivatives, e.g., theaflavins and thearubigins.
Green tea is thus less bfermentedQ and has the highest
quantity of tea catechins that are chemically defined as
flavan-3-ols. When the enzyme is allowed more time to act,
the tea will be fully fermented and most of the tea catechins
will be converted into theaflavins and thearubigins that give
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* Corresponding author. Tel.: +86 852 2819 9252; fax: +86 852 817
E-mail address: email@example.com (C.H. Cho).
European Journal of Pharmacology 500 (2004) 177–185
the characteristic aroma and colour of the black tea
(Balentine et al., 1997). Semi-fermented tea, e.g., Oolong
tea, has limited time of oxidation and is less fermented than
the black tea. In general, green tea contains about 30% w/w
of catechins in the dry leaves (Graham, 1992). The major
catechins, which are found in abundant proportion, are (?)-
epigallocatechin gallate, (?)-epigallocatechin, (?)-epicate-
chin and (?)-epicatechin gallate with (?)-epigallocatechin
gallate amounting to over 60% of the total catechins (Yang
and Koo, 1997). Other compounds obtainable in green tea
are the flavonols (quercetin, kaempferol and rutin), caffeine,
phenolic acids, theanine, and flavour compounds (Graham,
1992). Black tea contains less tea catechins (3–10% w/w),
while theaflavins and thearubigins account for about 2–6%
w/w and 10–20% w/w of the dry weight of the leaves,
respectively. Lung Chen tea and Pu-erh tea are typical
examples of Chinese green tea and black tea, respectively,
while Jasmine tea, Iron Buddha tea, Oolong tea are semi-
fermented Chinese teas. The catechin contents in these five
Chinese teas are presented in Table 1 and it was found that
Lung Chen green tea has the highest quantity of tea
catechins when compared with the semi-fermented and
black teas (Yang and Koo, 1997).
Green tea is commonly consumed in China, Japan and
Eastern Asia, while black tea is mainly brewed in European
countries and India. The intake of catechins can be expected
to be higher in the Asiatic countries and the health effects of
green tea may be more apparent when examined in the
Asian communities. The gastrointestinal tract is most likely
to be affected by tea drinking, since it has direct contact with
the tea solution and its components, usually in high
concentrations, irrespective of whether they are absorbed,
retained or re-circulated to the gut tissues. In this review, the
effects of green tea consumption on the gastrointestinal tract
will be explored to find out whether there is any co-relation
between green tea consumption and diseases of the gastro-
2. Diverse actions of tea catechins
Studies have shown that tea possesses diverse pharma-
cological properties which include anti-oxidative (Ho et al.,
1992, Serafini et al., 1996), anti-inflammatory (Mutoh et al.,
2000), anti-mutagenic (Kuroda and Hara, 1999; Steele et al.,
2000), anti-carcinogenic (Yang and Wang, 1993), anti-
angiogenic (Cao and Cao, 1999; Jung and Ellis, 2001),
apoptotic (Ahmad et al., 1997), anti-obesity (Dulloo et al.,
1999; Han et al., 1999), hypocholesterolemic (Yang and
Koo, 1997), anti-arteriosclerotic (Yang and Koo, 2000),
anti-diabetic (Zeyuan et al., 1998), anti-bacterial (Hu et al.,
2001), anti-viral (Clark et al., 1998; Mukoyama et al.,
1991), and anti-aging effects (Esposito et al., 2002).
However, these responses cannot always be reflected in
human studies. This may be due to the limited bioavail-
ability of tea components and the use of physiologically
unattainable tea concentrations in some of the animal and
in-vitro experiments. The unreliability of extrapolating and
applying results obtained in animal studies to humans
should also be contemplated.
In relation to the prevention of diseases by tea
consumption, many studies have demonstrated beneficial
effects of tea and catechins in the prevention of cancers
and cardiovascular disorders (Dufresne and Farnworth,
2000; Hertog et al., 1995; Imai and Nakachi, 1995;
Nakachi et al., 2000; NCI, DCPC, 1996). Findings from
epidemiological studies involving tea consumption have
suggested a chemopreventive effect of green tea on
gastrointestinal cancers and disorders when it is con-
sumed regularly in moderate to high quantity (Kuroda
and Hara, 1999; World Cancer Research Fund et al.,
1997; Zheng et al., 1996). However, some of the studies
conducted in the Western countries concerning the effects
of tea on gastrointestinal protection have demonstrated no
or negative results in cancer prevention, while promising
data were obtained mainly in studies performed in Asian
countries (Gao et al., 1994; Yang et al., 2001). This has
been suggested to be due to the consumption of a much
larger quantity of green tea by the Asian people while
the Westerners like to drink more black tea. Other factors
such as bias in subject selection, diets, alcohol con-
sumption, smoking (Lambert and Yang, 2003), types of
tea, total quantity of tea consumption, measurement errors
(Imai et al., 1997), temperature of the tea infusion (Wang
et al., 1996), and interactions of tea with other dietary
factors may influence the outcomes of the studies.
3. Mechanisms of action
The pharmacology and mechanisms of action of tea on
its anti-inflammatory and anti-cancer actions have been
reviewed in several publications (Bode and Dong, 2002;
Surh, 1999). Some suggested mechanisms for its suppres-
sive effects on inflammation and carcinogenesis have been
Types of Chinese tea with different degrees of fermentation and catechin
Types of teaDegree of
gallate (% w/w)
Jasmine tea7.48F0.49 12.72F0.70
Extracted from Yang and Koo (1997). Values are expressed as mean-
FS.E.M. of four to five determinations in weight percentage.
M.W.L. Koo, C.H. Cho / European Journal of Pharmacology 500 (2004) 177–185
depicted in Fig. 1. It is well known that green tea is a potent
antioxidant with anti-oxidative activity greater than vitamins
C and E (Wiseman, 1997). Besides acting as a scavenger for
reactive oxygen and nitrogen species, tea also enhances
expression of intracellular endogenous antioxidants such as
glutathione, glutathione reductase, glutathione peroxidase,
glutathione-S-reductase, catalase, and quinone reductase
(Khan et al., 1992; Valerio et al., 2001). All of these
activities prevent lipid peroxidation and damage to the DNA
structure. Green tea and (?)-epigallocatechin gallate also
bind to metal ions and further reduce the generation of
reactive free radicals (Hider et al., 2001; Morel et al., 1994).
In limiting the formation of carcinogens, green tea and its
catechins have been shown to promote the elimination of
procarcinogens, e.g., polycyclic hydrocarbons and hetero-
cyclic amines, from the body by inducing phase I
cytochromes P450 1A1, 1A2, and 2B1 enzymes and phase
II detoxification enzymes, e.g., glucuronosyl transferase
(Sohn et al., 1994). The procarcinogen activating enzyme
cytochrome P450 3A4 is also suppressed (Lin et al., 1999;
Muto et al., 2001). Furthermore, the formation of endoge-
nous N-nitroso compounds was found to be reduced by tea
consumption (Yang and Wang, 1993).
The chemopreventive effect of green tea and its catechins
on carcinogenesis have been attributed to their inhibition on
cell proliferation (Chen et al., 1998; Lea et al., 1993; Liang
et al., 1999; Valcic et al., 1996), cell cycle arrest (Liang et
al., 1999), blockade of growth factor receptors (Fujiki et al.,
1999; Liang et al., 1977), suppression of mitotic signals (Lin
et al., 1999), reduction in cytokines release (Fujiki et al.,
1999), inhibition of angiogenesis by interfering with the
activities of metalloproteinases, serine proteinases and
vascular endothelial growth factor (Jung et al., 2001),
prevention of nuclear factor kappa B and activator protein
1 activation (Ahmad et al., 2000; Lin and Lin, 1997),
inactivation of topoisomerase I (Berger et al., 2001) and
telomerase (Naasani et al., 1988) resulting in apoptosis.
(?)-Epigallocatechin gallate has been found to be a
potent inducible nitric oxide synthase and cyclooxygenase-2
inhibitor (Chan et al., 1997; Mutoh et al., 2000; Raso et al.,
2001). In suppressing the release of nitric oxide and
prostaglandins, which are important mediators for inflam-
mation and tumorogenesis, green tea can limit inflammatory
reactions and promotion of cancer. Recently, (?)-epigallo-
catechin gallate has been shown to bind to a specific
metastasis associated 67-kDa laminin receptor that is
expressed on a variety of tumor cells (Tachibana et al.,
2004). Green tea may then interfere with the promotion of
cancer by preventing metastasis of the tumour. Other factors
that are related to metastasis, e.g., urokinase plasminogen
activator (Kim et al., 2004), urokinase (Jankun et al., 1997),
and matrix metalloproteinases (Sazuka et al., 1997) were
also reported to be inhibited by green tea.
It has to be noted that some of the mechanistic studies
of tea catechins were performed in the concentration ranges
of 10–1000 AM, which is unlikely to be achieved under
physiological condition, except with the tissues in the
gastrointestinal tract, which comes into direct contact with
the tea solution. It has been found that the peak plasma
level of (?)-epigallocatechin gallate was only 0.17 AM
(77.9F22.2 ng/ml) after 1.6 h of oral consumption of a
green tea solution containing 195 mg (?)-epigallocatechin
gallate (Lee et al., 2002) and the plasma concentration of
(?)-epigallocatechin gallate was usually less than 1 AM
(Yang et al., 1998). This could provide a useful reference
value for future studies involving the use of cell cultures.
4. Bioavailability of green tea
Tea catechins are well absorbed after oral administration
(Nakagawa et al., 1997; Yang et al., 1998) and (?)-
epigallocatechin gallate is quite stable in the stomach and
small intestine. The content of (?)-epigallocatechin gallate
in the intestine was observed to increase sharply within a
few hours and was still present in the large intestine after 8 h
when a single dose of (?)-epigallocatechin gallate 50 mg
was administered to rats (Hara, 1997). Absorbed tea
catechins are biotransformed in the liver to conjugated
metabolites, i.e., glucuronidated, methylated, sulfated deriv-
atives. While (?)-epigallocatechin and (?)-epicatechin are
mainly conjugated, (?)-epigallocatechin gallate is usually
present in free form in human plasma (Chow et al., 2001).
Some of the catechins delivered to the gut can be
glucuronidated by the glucuronosyl transferase in the
mucosa of the intestine (Piskula and Terao, 1998). In the
Fig. 1. Postulated anti-inflammatory and anti-cancer actions of green tea and tea catechins.
M.W.L. Koo, C.H. Cho / European Journal of Pharmacology 500 (2004) 177–185
gut tissue h glucuronidases and microflora could also
convert the conjugated products to agylcones (Aura et al.,
2002). Some of them will be reabsorbed, while others will
be metabolized to form valerolactones, phenylacetic and
phenylpropionoic acids (Bravo, 1998; Li et al., 2000;
Meselhy et al., 1989). Thus tea catechins undergo enter-
ohepatic recirculation quite extensively (Nakagawa and
Miyazawa, 1997). After absorption, the catechins are widely
distributed in all body tissues with the highest concentration
found in the esophagus, intestine and colon (Lambert and
Yang, 2003; Yang et al., 2000). High levels of tea
polyphenols can be reached in the body when green tea is
frequently consumed (Suganuma et al., 1998).
5. Green tea and the aerodigestive sites
Green tea consumption has been reported to increase the
acid resistance of teeth to damage by cariogenic bacteria
(Gutman and Ryu, 1996; Hamilton-Miller, 2001). Green tea
was shown to inhibit the causative bacteria, which contrib-
ute to the formation of dental plague and caries. It has been
demonstrated that tea can inactive glucosyltransferase and
dextran sucrase thus inhibiting the formation of water-
insoluble glucan and lactic acid, respectively (Otake et al.,
1991). This reduced the adhesion of the causative bacteria
most noticeably Staphylococcus mutans (Sakanaka et al.,
1990), and Porphyromonas gingivalis (Sakanaka et al.,
1996) to the dental plaque. Its anticariogenic and antimic-
robe activities are related to the tea catechins and not due to
the action of its fluorine contents (Yu et al., 1995a,b). Tea
catechins, in particular (?)-epigallocatechin gallate, inactive
amylase in the saliva, and decrease hydrolysis of starch to
maltose thus reducing acid erosion on the teeth enamel
(Zhang and Kashket, 1998). Epidemiological studies
revealed a reduction in caries formation in tea drinking
populations and school kids from tea plantation areas in
Japan (Cao et al., 1987; Onisi, 1985, 1993), while subjects
given Oolong tea extract was observed to have less dental
plaque (Ooshima et al., 1994). Green tea can also clear up
bad breath by suppressing the growth of odour producing
bacteria (Suzuki, 1983; Ui, 1991).
Green tea has been found to be a potential chemo-
preventive agent for the treatment of oral leukoplakia, a
precursor lesion to oral cancer (Hsu et al., 2002). The
concentration of tea catechins in the saliva can reach a
higher value than in plasma (Yang et al., 1999). In vitro
studies demonstrated that green tea induced G1 cell cycle
arrest in oral leukoplaskia and promoted apoptosis in oral
squamous carcinoma cells. A study involving patients with
oral leukoplakias in Beijing found that tea catechins
treatment reduced the number of micronuclei and DNA
aberrations in the lymphocytes and reduced precancerous
mucosa lesions (Li et al., 1999).
The effect of green tea on esophageal cancer is not
consistent in that some reported a preventive effect while
others found an increase of incidence in esophageal cancer.
However, the worsening effect of tea on esophageal cancer
has been attributed to the consumption of high temperature
tea solutions rather than to the effect of tea. Inverse
relationships between green tea consumption and esoph-
ageal cancer were found in epidemiological studies done in
China. A study conducted in Jiangsu Province, China
demonstrated that the consumption of green tea in an
amount of more than 1 g/month reduced the risk of
esophageal and stomach cancers independent of the
detoxifying enzymes glutathione-S-transferases M1 and
glutathione-S-transferases T1 genotype polymorphisms
(Gao et al., 1994, 2002). Another large case control study
in South America reported that subjects drinking more than
500 ml/day of tea were also less likely to have esophageal
cancer (Castellsague et al., 2000). It is possible that the
catechins particularly (?)-epigallocatechin gallate inhibit
the initiation and promotion phases of cancer development
by preventing free radical damage to DNA. Its anti-
angiogenic effect may account for its suppression of
growth of cancerous tissues by limiting their blood supply
and inhibition of cancer development (Cao and Cao,
1999). The metastasis of cancer has also been demon-
strated to be suppressed by green tea, which reduced the
expression of adhesion molecules and metalloproteinases
(Garbisa et al., 2001). Finally, green tea induces apoptosis
in cancer cells and prevents the promotion of cancer
(Ahmad et al., 1997).
6. Green tea and the stomach
Epidemiological studies have shown an inverse relation-
ship of green tea consumption with risk of gastric cancers.
The risk of stomach cancer decreases with the quantities of
tea consumed (Gao et al., 2002; Inoue et al., 1998; Ji et al.,
1996; Kono et al., 1988; Nakachi et al., 2000; Oguni et al.,
1992; Setiawan et al., 2001; Yu and Hsieh, 1991; Yu et al.,
1995a,b). The mechanisms may involve the inhibition of the
growth of Helicobacter pylori, the causative microorganism
in gastric carcinogenesis and the development of gastric and
duodenal ulcers (Graham et al., 1992). Tea catechins,
particularly (?)-epigallocatechin gallate, inactivate the
urease enzyme (Matsubara et al., 2003; Yee and Koo,
2000) for the conversion of urea into ammonia that buffers
the bacteria from digestion by gastric juice, and thereby
suppress proliferation of bacteria (Tsujii et al., 1992). This
activity of tea can be achieved in the cup of tea
concentrations and the minimum inhibitory concentrations
(50% to 90%) for Lung Chen Chinese green tea were found
to be between 0.125% w/v and 0.25% w/v (Yee and Koo,
2000). An inverse relationship was also found in a study
involving the evaluation of patients with gastric disorders
with their Chinese tea drinking habit (Yee et al., 2002). It
was observed that the incidence of infection with H. pylori
was lower in subjects who consumed tea regularly. Similar
M.W.L. Koo, C.H. Cho / European Journal of Pharmacology 500 (2004) 177–185
results were reported in animal studies confirming an anti-
H. pylori effect of tea and the active principles were
demonstrated to be the tea catechins (Matsubara et al.,
2003). Green tea also prevents chronic active gastritis and
lowers stomach cancer risk (Kuwahara et al., 2000;
Setiawan et al., 2001; Shibata et al., 2000).
Another important factor contributing to gastric carcino-
genesis is the challenge of nitrogenous mutagens and
heterocyclic amines in the stomach. Endogenously formed
N-nitroso compounds can increase the risk of gastric and
esophageal cancers (Mirvish, 1995). Nitrosation occurs in
the stomach and other part of the gut between amine and
amide precursors and nitrite generated from nitrate (Leach et
al., 1987). Tea catechins reduce N-nitroso compound
formation by reacting with the nitrosating species and self
oxidized to quinone (Bartsch et al., 1988). This reduces the
gastric levels of nitrosating substances and inhibits the
nitrosation of susceptible secondary amines and amides to
carcinogenic nitrosamines and nitrosamides (Tanaka et al.,
1998). Results obtained from human studies have demon-
strated the inhibition of formation of a non-carcinogenic test
compound N-nitrosoproline from nitrosation of proline by
daily intake of 3 to 5 g of green tea (Stich, 1992; Wu et al.,
1993; Xu et al., 1993). Heterocyclic amines present in
cooked meats are known carcinogens and green tea inhibits
the formation of heterocyclic amines (Weisburger et al.,
1994). Tea promotes the biotransformation of these com-
pounds to excretable products through enhanced expression
of conjugating enzyme, glucuronyl transferase, which is
involved in the glucuronidation of heterocyclic amines
(Dashwood et al., 1999). Indeed, results from animal study
demonstrated the inhibition of chemically induced forest-
omach cancer in mice treated with tea (Yang and Wang,
1993). Table 2 summarized some of the possible mecha-
nisms of action of green tea in the prevention of gastro-
7. Green tea and the intestine
Antimicrobial activities of tea have been well demon-
strated (Diker et al., 1991; Sugita et al., 1999; Toda et al.,
1991), and tea has been shown to inhibit the growth of
Vibrio cholerae, Salmonella typhi, Campylobacter jejuni,
Campylobacter coli, H. pylori, Shigella, Salmonella,
Clostridium pseudomonas, Candida, Mycoplasma and
Cryptococcus. Thus, tea may modify the intestinal micro-
flora. There are studies supporting a role of green tea in
modulating microflora in the intestine by selectively
increasing the growth of bifidobacteria and lactobacilli
(acidophytes) in the gut wall (Weisburger, 1999; Yama-
moto et al., 1997). This reduces the formation of ammonia,
skatole, harmful amines procarcinogens in the large
intestine and the carcinogenic load on the intestine. The
production of acids is also lowered leading to a decrease in
the pH value of the feces (Yamamoto et al., 1997).
Therefore, bacteria profile in the intestine can be modu-
lated by tea drinking and tea may affect the carcinogenic
process in the intestine.
Green tea has been found to inhibit the expression of
cyclooxygenases and inducible nitric oxide synthase in
colonic tissues, which are constantly found to be elevated
in subjects with ulcerative colitis (Hendel and Nielsen,
1997) and colorectal cancers (Kutchera et al., 1996; Sano
et al., 1995). The suppression of cyclooxygenase-2 by
non-steroidal anti-inflammatory drugs, e.g., sulindac, has
been found to reduce cancer development in patients with
large bowel adenoma (Giovannucci et al., 1995; Green-
berg et al., 1993; Nugent et al., 1993). Green tea
polyphenols consistently inhibit cyclooxygenase-2 activity
in human colon tumour tissues (Hong et al., 2001) and
tea co-administration produces an enhancing effect with
the cyclooxygenase inhibitors (Ohishi et al., 2002;
Suganuma et al., 1999). Similar synergistic effect of
(?)-epigallocatechin gallate with sulindac co-administra-
tion was observed in multiple intestinal neoplasia (Min)
mice which has a germline mutation of the murine
adenomatous polyposis coli gene and develops intestinal
tumors similar to the familiar adenomatous polyposis
patients (Fujiki et al., 2003).
An inverse relationship to colorectal cancer risk was
observed with green tea consumption (Kato et al., 1990).
A protective effect on rectal cancer incident was also
observed in Chinese females from Hebei who drink tea
regularly (Zheng et al., 2002). A population study in
Japan found that there was a delay in cancer occurrence
in subjects consuming green tea (Imai et al., 1997). The
incidence of colorectal cancer was found to be lower in
patients who had consumed over 10 cups of green tea
per day (Nakachi et al., 2000). A threshold quantity for
the protective effect of tea may exist, since no significant
difference was observed in subject drinking less than 10
cups a day. This dose–response relationship was also
reported in a case control study on black tea consumption
Possible mechanisms of action for green tea to prevent gastrointestinal
Mechanisms of action References
(A) Growth inhibition of
Matsubara et al. (2003)
Yee and Koo (2000)
Yee et al. (2002)
Setiawan et al. (2001)
Shibata et al. (2000)
Bartsch et al. (1988)
Tanaka et al. (1998)
Wu et al. (1993)
Xue et al. (1993)
Sohn et al. (1994)
Yang and Wang (1993)
Fujiki et al. (2003)
Hong et al. (2001)
Ohishi et al. (2002)
Suganuma et al. (1999)
Yamamoto et al. (1997)
(B) Prevention of chronic
(C) Reduction of N-nitroso
(D) Decrease conversion of
mutagens to carcinogens
(E) Suppression of
inducible nitric oxide
(F) Modification of
microflora in the intestine
M.W.L. Koo, C.H. Cho / European Journal of Pharmacology 500 (2004) 177–185
and risk of rectal cancer in Moscow (Il’yasova et al.,
2003). It has been proposed that (?)-epigallocatechin
gallate at physiological concentrations arrests cell growth
at Go/G1 phase by inhibiting topoisomerase I activity and
induces apoptosis in several human colon carcinoma cell
lines. These findings suggest that it could be combined
with other anticancer drugs in the treatment of colon
cancer (Berger et al., 2001).
Green tea may exert a protective effect on the gastro-
intestinal mucosa. In a study involving the induction of
mucosal damage by fasting in rats, the administration of
0.6% w/w green tea was shown to prevent atrophy of the
intestinal mucosa and promote healing of mucosal damage.
It is suggested to be mediated by the antioxidant activity of
tea catechins thus may prevent bacterial and toxin trans-
location in critically ill or nutritionally depleted patients
(Safar et al., 2003).
The absorption of fat and sugar was found to be
reduced by tea consumption. Tea has been shown to
inhibit digestive lipases (Han et al., 1999; Juhel et al.,
2000) and interfere with lipid-micelle formation in the
intestine (Ikeda et al., 1992) leading to a decrease in fat
absorption. These effects coupled with its upregulation on
low density lipoprotein receptor through inhibition on
proteasome activity (Bursill et al., 2001; Kuhn et al.,
2004) contribute to its lipid lowering effect. Studies have
also shown that tea lowered the uptake of sugar and
reduced blood sugar level through suppression on glucose
transporter activity in the intestinal epithelium (Shimizu,
1999). This may be beneficial to diabetes subjects in
lowering their blood sugar levels.
A trial on the effect of tea catechins in bowel movements
in healthy volunteers has demonstrated an improvement of
the bowel activity after taking 500 mg (?)-epigallocatechin
gallate tablets for 3 months. The bowel movements became
more regular and this may be attributed to the inhibition of
a-amylase and the modulating effects of tea catechins on the
fecal flora (Hara, 1997).
8. Overall perspectives
Tea is widely consumed worldwide and it is without
observable side effects even when taken chronically
(Graham, 1992). Epidemiologic studies have suggested
an inverse relationship of green tea consumption with
gastric and colorectal cancers. In Japan, green tea has
already been promulgated as a chemopreventive beverage.
Further investigations relating to the health effects of tea
drinking are now being conducted, and this may help to
clarify the usefulness of green tea in disease prevention. Tea
catechins were shown to act synergistically with each other
and with caffeine in their disease-modifying actions. Thus,
unfractionated green tea solution is more beneficial than
individual tea catechin component if one has to harvest the
potential health promoting effects of green tea in the
prevention of gastrointestinal diseases (Fujiki, 1999; Suga-
numa et al., 1999).
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