Ip. Lee et al., CHEMOPREVENTIVE EFFECT OF GREEN TEA (CAMELLIA-SINENSIS) AGAINST CIGARETTE SMOKE-INDUCED MUTATIONS (SCE) IN HUMANS, Journal of cellular biochemistry, 1997, pp. 68-75
Green tea (Camellia sinensis) is consumed daily between the meals or a
fter meals in Japan and other Asian countries. In recent years, green
tea and its major polyphenolics have been demonstrated to prevent chem
ically induced tumors in a variety of experimental animal models syste
m. The exact mechanism(s) of its anticarcinogenic activity remains to
be elucidated, but green tea polyphenolics have demonstrated antimutag
enic, anticarcinogenic, antioxidant and antipromotional effects, inclu
ding inhibition of Phase I and inducing Phase II enzymes. Enzyme activ
ities of glutathione peroxidase, catalase, and quinone reductase, and
glutathione S-transferase are also induced. However, a paucity of gree
n tea effects in humans prompted us to investigate antimutagenic effec
ts of green tea against smoke-induced mutation in humans. Chemoprevent
ive effects of green tea and coffee among cigarette smokers were exami
ned in 52 clinically healthy male subjects between 20-51 years of age.
Blood specimens were obtained from non-smokers (Croup I), smokers (II
), smokers consuming green tea (III), and smoker/coffee drinkers (IV).
The mean years of cigarette smoking (>10 cigarettes/day) of Groups II
, III, and IV ranged from 13.4-14.7 years. Daily intake of green tea a
nd coffee was 3 cups/day/6 months (III and IV). The frequencies of sis
ter-chromatid exchange (SCE) in mitogen-stimulated peripheral lymphocy
tes from each experimental group were determined and statistically ana
lyzed. SCE rates were significantly elevated in smokers (9.46 +/- 0.46
) vs. non-smokers (7.03 +/- 0.33); however, the frequency of SCE in sm
okers who consumed green tea (7.94 +/- 0.31) was comparable to that of
non-smokers, implying that green tea can block the cigarette-induced
increase in SCE frequency. Coffee, by contrast, did not exhibit a sign
ificant inhibitory effect on smoking-induced SCE. (C) 1998 Wiley-Liss,
Inc.