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Laboratory for Cancer Research, College of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854
3To whom correspondence and reprint requests should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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KEY WORDS: • tea • polyphenols • cancer chemoprevention • animal models • cancer cell lines
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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Tea constituents and their biochemical properties |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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). The structures of the major
catechins and black tea polyphenols are shown in Figure 1
. EGCG is the most abundant catechin and has received by far the most
attention. Flavonols such as quercetin and their glycosides exist at
lower levels. Caffeine usually accounts for 3–6% of the dry weight of
brewed tea. In the manufacture of black tea, the tea leaves are crushed
to allow the polyphenol oxidase to catalyze the oxidation and
polymerization of catechins in a process known as "fermentation."
Some of the catechins remain, accounting for 3–10% of the dry weight
in brewed black tea. Theaflavins, which include theaflavin,
theaflavin-3-gallate, theaflavin-3'-gallate and
theaflavin-3,3'-digallate, are key to the characteristic color and
taste of black tea and account for 2–6% of the dry weight in brewed
black tea. The major fractions of black tea polyphenols, generally
known as thearubigens, have higher molecular weights and are poorly
characterized chemically; they account for >20% of the solid weight
of brewed black tea (Balentine et al. 1997
). Of all the
tea produced world-wide, 78% is black tea, which is usually
consumed in the Western countries, 20% is green tea which is commonly
consumed in Asian countries such as China and Japan, and 2% is Oolong
tea which is produced (by partial fermentation) mainly in southern
China.
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). Green and black tea and tea polyphenols have been
shown to scavenge reactive oxygen and nitrogen species and reduce their
damage to lipid membranes, proteins and nucleic acids in cell-free
systems. Tea polyphenols are known to bind to proteins, as exemplified
by their binding to the proline rich salivary proteins (Haslam 1996
). At low concentrations of tea polyphenols, this binding
property may affect certain enzymes, receptors and membrane activities
specifically, resulting in the different biological activities observed
by different investigators. |
Inhibition of carcinogenesis by tea in animal models |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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, Dreosti et al. 1997
,
Katiyar and Mukhtar 1996
, Yang and Wang 1993
, Yang et al. 1996
and 1999
). For example,
inhibition of lung tumorigenesis by tea preparations has been
demonstrated in A/J mice that have been treated with the tobacco
carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).
Administration of decaffeinated green or black tea to mice during the
NNK treatment period, or after the NNK treatment period, markedly
reduced the number of tumors formed in the mice (Wang et al. 1992a
). The inhibitory activity of black tea
theaflavins was also demonstrated in this model (Yang et al. 1997a
). When the mice were given black tea 16 wk after
the NNK injection, at which time almost all of the mice had developed
adenomas, the progression of these tumors to adenocarcinomas was
significantly inhibited (Yang et al. 1997a
). Brewed
black tea and green tea infusions, when given to A/J mice as the sole
source of drinking fluid, also inhibited spontaneous lung tumorigenesis
(Landau et al. 1998
). The inhibitory action of caffeine
against lung tumorigenesis has been demonstrated previously in mice
(Xu et al. 1992
) and in rats (Chung et al. 1998
). In the latter study, caffeine, at a concentration
corresponding to that in a 2% black tea extract, displayed inhibitory
activity comparable to, or stronger than that of 2% black tea. The
above experiments indicate that tea has broad inhibitory activity
against both spontaneous and chemically induced lung tumorigenesis and
is effective when administered during the initiation, promotion or
progression stages of carcinogenesis. This conclusion may also apply to
other animal models such as chemically and UV light–induced skin
carcinogenesis (Huang et al. 1997
, Katiyar and Mukhtar 1996
, Wang et al. 1992b
and 1994
).
Conflicting results have been reported concerning the effects of tea on
colon carcinogenesis. Colon cancer formation induced by azoxymethane in
rats and by 1,2-dimethylhy-drazine in mice was inhibited by low
concentrations of green tea polyphenols (0.01 or 0.1% solution as
drinking fluid) and EGCG (reviewed in Yang et al. 1996
).
On the other hand, treatment of rats with black tea (0.6–2.5%
solution) in drinking fluid did not inhibit azoxymethane-induced
colon carcinogenesis (Weisburger et al. 1998
). One
possible interpretation of these two different types of results is that
green tea polyphenols inhibit colon carcinogenesis, whereas some black
tea constituents are much less effective. The effect of tea on mammary
carcinogenesis was not demonstrated in several studies. In a recent
study, black tea (1.25 or 2.5% solution) was found not to inhibit
7,12-dimethylbenz[a]anthracene-induced mammary gland tumorigenesis in
rats fed an AIN-76A diet, but to reduce mammary tumorigenesis in rats
fed a high fat diet (Rogers et al. 1998
). On the other
hand, EGCG has been shown to inhibit the growth of human breast and
prostate cancer cells in athymic mice (Liao et al. 1995
).
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Effects of tea consumption on human cancers |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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, Buschman 1998
, Katiyar and Mukhtar 1996
, Yang and Wang 1993
, Yang et al.
1996). For example, studies in northern Italy have suggested a
protective effect of tea against oral, pharyngeal and laryngeal cancer.
In a case-control study in Shanghai, frequent consumption of green
tea was shown to be associated with a lower incidence of esophageal
cancer, especially among nonsmokers and nondrinkers of alcohol. Similar
studies in Shanghai have suggested that green tea consumption is
associated with lower risk of pancreatic and colorectal cancer. The
protective effect against gastric cancer by tea has also been suggested
from studies in Kyushu (Japan), northern Turkey, and central Sweden,
but not from many other studies in different geographic areas
(Yang et al. 1996
). In studies in Saitama, Japan, women
consuming >10 cups of tea daily were shown to have lower risk for
cancer (all sites combined) and increased tea consumption was
associated with lower risk for breast cancer metastasis and recurrence
(Imai et al. 1997
, Nakachi et al. 1998
).
In a prospective cohort study of postmenopausal women in Iowa, tea
(mostly black tea) drinking was shown to be associated with a lower
risk for digestive tract cancers and urinary tract cancers
(Zheng et al. 1996
). On the other hand, in the
Netherlands Cohort Study on Diet and Cancer, consumption of black tea
was not found to affect the risk for stomach, colorectal, lung and
breast cancers (Goldbohm et al. 1996
). A recent study of
middle-aged Finnish men indicated a positive association between
increased tea consumption and colon cancer risk (Hartman et al. 1998
).
It appears that most reports on the cancer prevention effects were from
studies of Asians, who drink predominantly green tea, whereas studies
of black tea–drinking Europeans observed a protective effect
infrequently. The reviews on green tea and human cancer by
Buschman (1998)
and on black tea and cancer by
Blot et al. (1997)
seem to be consistent with this
suggestion. One possibility is that the cancer prevention activity of
green tea is stronger than that of black tea. In studies on the
inhibition of cancer formation by tea in animal models, the effective
components appear to be catechins, theaflavins and caffeine. Although
black tea contains all three classes of compounds, its catechin content
is much lower than that of green tea. The bioavailability and
biological activity of the major components of black tea, thearubigens,
are not known. It is also possible that the different results on tea
and cancer are due to the different etiological factors involved in
different geographic areas (Yang and Wang 1993
).
The lack of a clear-cut conclusion concerning the protective effect of tea against cancer in humans is in contrast to the conclusions obtained from animal studies. Some possible reasons for this difference are as follows: 1) tea may have a weak protective effect, but it is masked by confounding factors associated with life style in certain populations; 2) the amount of tea consumed by humans is much lower than the tea concentrations used in animal studies and therefore cannot produce a significant effect; and 3) tea inhibits carcinogenesis in animals by mechanisms that may not be applicable to the prevention of human cancer. To address these points, information on the active components, their bioavailability and tissue levels, and their mechanisms of action is of great importance.
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Absorption and tissue distribution of tea polyphenols |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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The absorption and tissue distribution of tea catechins are just beginning to be understood. After intravenous injection of decaffeinated green tea (DGT) into rats, the plasma concentration-time curves of EGCG, EGC and EC could be fit into a two-compartment model. The ß elimination half-lives (t1/2ß) were 212, 45 and 41 min for EGCG, EGC and EC, respectively. When pure EGCG was given intravenously., however, a shorter t1/2ß (135 min) for EGCG was observed, suggesting that other components in DGT could affect the plasma concentration and elimination of EGCG. After intragastric administration of DGT, ~14% of EGC and 31% of EC appeared in the plasma, but <1% of EGCG was bioavailable. Conversion of intragastrically administered EGCG to EGC was not observed. After intravenous administration of DGT, the level of EGCG was found to be the highest in the intestines, whereas the highest levels of EGC and EC were observed in the kidney.
When tea (0.6% green tea polyphenols) was administered to rats through the drinking fluid, the blood levels of EGC and EC were much higher than that of EGCG (unpublished results). A large amount of EGCG was found in the feces. The blood EGC and EC levels increased in the first 2 wk (peaked at 800-1000 µg/L), and then the levels decreased markedly to 300–350 µg/L on d 28. A similar decrease in urinary excretion of EGC and EC was also observed. When a second cycle of tea administration was initiated after a 10-d washout period, the EGC and EC levels were much lower than the high levels found on d 8 and 14 in the first cycle. After administration of tea to the rats for 8 d, substantial amounts of EGC and EC were found in the rat esophagus (185–195 ng/g tissue) large intestine (300–930), kidney (400–500), bladder (800–810), lung (190–230), and prostate (240–250), but the levels of EGC and EC were low in the liver, spleen, heart and thyroid. The amount of EGCG was higher in the esophagus and large intestine because of direct contact, but lower in other organs because of poor systemic absorption of EGCG by rats. A similar pattern of increase and then decrease in blood catechin levels was also seen in mice, except that the decrease took place 4 d after treatment with tea. In mice, the bioavailability of EGCG was much higher than that in rats. The highest levels of EGCG and other catechins were in the low micromolar range.
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Blood and saliva levels in humans |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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). These values were
observed at 1.4–2.4 h after the ingestion of the tea preparation. A
good dose-response relationship was not observed between the doses
of 3 and 4.5 g. The half-life of EGCG (5.0–5.5 h) appeared to
be higher than those of EGC and EC (2.5–3.4 h). EGC and EC (and lower
levels of EGCG in some individuals) were excreted through the urine.
Over 90% of the total urinary EGC and EC was excreted within 8 h.
Substantial amounts of the catechins were detected in colon mucosa and
prostate tissues in surgical samples from patients who consumed tea
12 h before surgery. The results suggest that in heavy tea
drinkers (e.g., five cups green tea per day), the plasma levels of
catechins are comparable to those found in mice used in cancer
prevention studies with tea.
Because of the possible application of tea in the prevention of oral
and esophageal cancers, the salivary levels of tea catechins were
determined in six human volunteers after drinking tea (Yang et al. 1998a
). Saliva samples were collected after the mouth was
rinsed thoroughly with water. After drinking green tea preparations
(equivalent to 2–3 cups of tea), peak saliva levels of EGC (11.7–43.9
mg/L), EGCG (4.8–22 mg/L) and EC (1.8–7.5 mg/L) were observed after a
few minutes. These levels were two orders of magnitude higher than
those in the plasma. The t1/2 of the salivary
catechins was 10–20 min, much shorter than that of the plasma. Holding
a tea solution in the mouth for a few minutes (without swallowing)
produced even higher salivary catechin levels, but taking tea solids in
capsules resulted in no detectable salivary catechin level. Holding
EGCG solution in the mouth resulted in EGCG and EGC in the saliva and
subsequently EGC in the urine. The results suggest that EGCG was
converted to EGC in the oral cavity, and both catechins were absorbed
through the oral mucosa. A catechin esterase activity that converts
EGCG to EGC was found in the saliva (Yang et al. 1998a
).
The results suggest that slowly drinking tea is a very effective way of
delivering rather high concentrations of catechins to the oral cavity
and then the esophagus.
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Studies with cell lines |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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. The efficacy of inhibition varied, depending on the cell line used.
EGCG was generally the best inhibitor in most of the cell lines tested,
with 50% inhibition (IC50) values ranging
between 22 and 130 µmol/L. EGC and GC were better
inhibitors toward A427 cells with IC50 values of
34 and 38 µmol/L, respectively. Our laboratory has also
shown that EGCG and EGC inhibit the growth of H661 and H1299 with
IC50 values of 22 µmol/L. The growth
inhibition of Ha-ras–transformed 21 BES cells by the black tea
polyphenol, theaflavin-3–3'-digallate, was similar to the growth
inhibition caused by green tea polyphenols, EGCG and EGC (Yang et al. 1998b
). These studies demonstrate the biological
activities of tea polyphenols, but the effective concentrations
observed are generally 1–2 orders of magnitude higher than peak human
plasma concentrations. The lowest effective concentration of EGCG (1–2
µg/L) observed was in the inhibition of the transformation
of preneoplastic human mammary epithelial cells by benzo[a]pyrene
(Katdare et al. 1998
).
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) (Ahmad et al. 1997
,
Hibasami et al. 1996
and 1998
, Okabe et al. 1997
, Yang et al. 1998b
). EGCG may also act as a
prooxidant through H2O2
production to induce apoptosis. Addition of catalase into the culture
media inhibited EGCG-induced apoptosis (Yang et al. 1998b
). In combination with other chemopreventive drugs such as
sulindac and tamoxifen, EGCG induced a synergistic apoptotic effect
(Suganuma et al. 1999
). Other mechanisms for the growth
inhibition of cancer cells may be through the induction of cell cycle
arrest by EGCG and the inhibition of signal transduction pathways
leading to the activation of important transcription factors activator
protein 1 (AP-1) and nuclear factor 
B (NF-B) (Ahmad et al. 1997
, Dong et al. 1997
, Lin and Lin 1997
, Okabe et al. 1997
). |
Possible active components and their bioavailability |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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, Katiyar and Mukhtar 1996, Xu et al. 1992
, Yamane et al. 1995
). However, other
components should also be considered on the bases of their biological
activities and bioavailabilities. For example, EGC, which is also
abundant in green tea, is more bioavailable; it has antiproliferative
and inhibitory activities similar to those of EGCG and could also be
important.
From our studies with three human lung cancer cell lines (H661, H1299
and H441) and one colon cancer cell line (HT-29), we observed that the
potency of inhibiting cell growth by green tea polyphenols had the rank
order of EGCG = EGC > ECG > EC (Yang et al. 1998b
). The potency of theaflavin-3–3'-digallate was similar
to that of EGCG and higher than that of theaflavin-3 (3')-gallate,
which was still higher than theaflavin. The growth inhibitory activity
of green tea extracts appeared to be due to the summation of activities
of EGCG, EGC, ECG and EC. These catechins, together with the
theaflavins, may account for most of the growth inhibitory activity of
black tea extracts. The growth inhibitory activity of thearubigens, the
major components of black tea, is not known.
The inhibition of EGCG against skin, stomach, colon, and lung
carcinogenesis(Chung et al. 1998
, Xu et al. 1992
, Yamane et al. 1995
) as well as the growth
of human prostate and breast tumors in athymic mice have been
demonstrated (Liai et al. 1995
). Theaflavins have been
shown to inhibit lung and esophageal carcinogenesis (Morse et al. 1997
, Yang et al. 1997a
). The
activity of EGC has not been tested in carcinogenesis models, but
short-term studies showed that it has about the same
antiproliferative activity as EGCG (unpublished results). In many
studies, black tea has comparable or slightly lower inhibitory
activities. The results suggest that the remaining catechin in black
tea, the theaflavins, and other components in black tea all contribute
to the cancer inhibitory activity. The bioactivity of thearubigens in
animals is not known. The inhibitory activity of another constituent in
tea, caffeine, has been demonstrated in different animal models
(Chung et al. 1998
, Huang et al. 1997
,
Xu et al. 1992
).
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Possible mechanisms for the inhibitory actions of tea on tumorigenesis |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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, Yang 1997
), in the
search for relevant mechanisms, it is necessary to consider the tissue
concentrations of the effective components. Inhibitory activities
elicited by low micromolar or lower concentrations are likely to be
more relevant than activities demonstrated with higher concentrations
of tea components. Many studies have demonstrated the inhibition of
carcinogen activation by tea and tea polyphenols in vitro, but such
activities have been observed only in some studies in vivo. Moderate
enhancement of glutathione peroxidase, catalase, glutathione
S-transferase, NADPH-quinone oxidoreductase, UDP-glucuronosyl
transferase and methoxyresorufin O-dealkylase activities by
tea administration has also been reported (Bu-Abbas et al. 1994
, Khan et al. 1992
, Sohn et al. 1994
); the effects of these enzyme inductions on carcinogenesis
are not clear.
Reactive oxygen species may play important roles in
carcinogenesis through damaging DNA, altering gene expression, or
affecting cell growth and differentiation (Cerutti 1989
,
Feig et al. 1994
). The anticarcinogenic activities of
tea polyphenols are believed to be related, but not due entirely to
their antioxidative properties. The findings that green tea polyphenol
fractions inhibited 12-O-tetradecanoylphorbol-13-acetate
(TPA)-induced hydrogen peroxide formation in mouse epidermis
(Huang et al. 1992
) and 8-hydroxydeoxyguanosine
formation in different systems (Bhimani et al. 1993
,
Xu et al. 1992
) are consistent with this concept. On the
other hand, the prooxidant activity of tea polyphenols may play a role
in inducing apoptosis. In the induction of apoptosis with human lung
cancer H661 cells by EGCG, the activity could be inhibited by catalase
(Yang et al. 1998b
). Inhibition of tumor
promotion–related enzymes, such as TPA-induced epidermal ornithine
decarboxylase (Hunag et al. 1992
, Wang et al. 1991
, protein kinase C (Yoshizawa et al. 1992
,
lipoxygenase and cyclooxygenase (Katiyar et al. 1992
,
Lou 1987
), by tea preparations has been demonstrated.
Recently, we demonstrated that green tea administration to normal human
subjects resulted in a rapid decrease in prostaglandin
E2 (PGE2) levels in rectal
biopsy tissues (August et al. 1999
). Other mechanisms,
relating to the quenching of activated carcinogens (Khan et al. 1988
), antiviral activity (Shimamura 1994
) and
enhancement of immune functions (Yan 1992
) have also
been suggested, but their relevance to carcinogenesis is unknown.
Inhibition of nitrosation by tea preparations has been demonstrated in
vitro and in humans (Nakamamura and Kawabata 1981
,
Stich 1992
), and this may be an important factor in the
prevention of certain cancers, e.g., gastric cancer, if the
endogenously formed N-nitroso compounds are causative
factors.
The inhibitory activities of tea and tea polyphenols may be due in many
cases to their ability to inhibit growth-related signal
transduction pathways. For example, EGCG and theaflavins inhibit
epidermal growth factor– or TPA-induced transformation of JB6
cells, and this inhibition was correlated with the inhibition of
AP-1–dependent transcriptional activity (Dong et al. 1997
). The inhibition of AP-1 activation occurs through the
inhibition of a c-jun NH2-terminal
kinase–dependent pathway. In H-ras–transformed JB6 (the 30.7b Ras 12
cells), the H-ras–activated AP-1 pathway is a major growth stimulant.
In these cells, the AP-1 activation was inhibited by EGCG, EGC,
theaflavin-3,3'-digallate and other polyphenols, and the
phosphorylation of both c-jun and an extracellular
signal-regulated protein kinase (Erk) was inhibited (unpublished
results). Because the ras genes are activated in many animal
carcinogenesis models and in human cancers, the inhibition of the
phosphorylation of c-jun and Erk could be an important mechanism
for the inhibition of cancer formation and growth. A recent study by
Cao and Cao (1999)
demonstrated that EGCG can inhibit
angiogensis by inhibiting the growth of endothelial cells. In addition,
the administration of 1.25% green tea as the drinking fluid to mice
injected with vascular endothelial growth factor reduced corneal
neovascularization significantly by 35–70%. This can be a potent
mechanism for the inhibition of cancer growth in vivo. Inhibition of
tumor necrosis factor 
has also been proposed as a possible
mechanism for the cancer preventive activity of EGCG (Suganuma et al. 1996
). The inhibition of NF-B by EGCG, which has been
demonstrated recently (Lin et al. 1997
), may also
contribute to the anticarcinogenic effect of tea polyphenols in many
situations.
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SUMMARY |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by National Institutes of Health grant CA56673.
4 Abbreviations: AP-1, activator protein 1; DGT, decaffeinated green tea; EC, (-)-epicatechin; ECG,
(-)-epicatechin-3-gallate; EGC, (-)-epigallocatechin; EGCG,
(-)-epigallocatechin-3-gallate; IC50, concentration at
which 50% inhibition occurs; NF-B, nuclear factor B; NNK,
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; TPA, 12-O-tetradecanoylphorbol-13-acetate.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONTea constituents and their...Inhibition of carcinogenesis by...Effects of tea consumption...Absorption and tissue...Blood and saliva levels...Studies with cell linesPossible active components and...Possible mechanisms for the...SUMMARYREFERENCES |
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