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Mechanisms of inhibition of carcinogenesis by tea
Author(s) -
Yang Chung S.,
Chung Jee Y.,
Yang GuangYu,
Li Chuan,
Meng Xiaofeng,
Lee MaoJung
Publication year - 2000
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520130113
Subject(s) - theaflavin , polyphenol , chemistry , carcinogenesis , mapk/erk pathway , biochemistry , catechin , cell growth , apoptosis , glucuronide , tumor promotion , gallate , kinase , pharmacology , biology , metabolism , antioxidant , nuclear chemistry , gene
Tea ( Camellia sinensis ) preparations have been shown to inhibit tumorigenesis at the initiation, promotion, and progression stages in different animal models. The anti‐proliferative effects of tea polyphenols may be a key mechanism, especially in the NNK‐induced lung tumorigenesis model with mice. Studies with cell lines have demonstrated that tea polyphenols inhibit cell proliferation and induce apoptosis. The effective concentrations used in these studies (20–100 μM) are usually higher than those observed in blood and tissues of humans and animals, which are in the low micromolar range. Glucuronide and sulfate conjugated and methylated catechins as well as ring fission products (due to intestinal microflora) have been observed in human plasma and urine. Purified green and black tea polyphenols inhibited the H‐ ras induced mitogen‐activated protein kinases, AP‐1 activities, and the growth of 30.7b Ras 12 and BES21 cells. Among the catechins, both the galloyl structure on the B ring and the gallate moiety are important for the inhibition. Both (‐)‐epigallocatechin‐3‐gallate and theaflavin‐3,3′‐digallate inhibited the phosphorylation of c‐jun and p44/42 (ERK 1/2). More mechanistic and human studies in these areas will help us to understand the possible inhibitory action of tea against carcinogenesis in humans.