Prevention of carcinogenesis by tea polyphenols*^†

Abstract

Tea, an extract of the leaves of the plant Camellia sinensis, has been considered a medicine and healthful beverage for ages. The beneficial effects of tea are thought to be due to its polyphenolic components. Herein, we discuss the present status of tea as a possible cancer chemopreventive agent, covering basic chemistry and biochemical activity of tea, pharmacokinetics of major tea components, studies in animal and cell lines, epidemiological investigations, and future challenges. Tea is one of the few chemopreventive agents known to have protective effects at different stages of the carcinogenic process. Tea constituents may inhibit this process by modulating signal transduction pathways leading to the inhibition of cell proliferation and transformation and enhancement of apoptosis. These activities may or may not be due to the antioxidative activity of tea polyphenols. The bioavailability and tissue levels of tea polyphenols is a key topic to be studied in order to understand the mechanisms of action of tea and its possible protection against cancer in humans.

Key Words :

• Tea
• Biotransformation
• Carcinogenesis

Abbreviations:
EGCG	=	(−)-epigallocatechin gallate
ECG	=	(−)-epigallocatechin
EC	=	(−)-epicatechin
ECG	=	(−)-epicatechin gallate
M4	=	[5-(3′,4′-dihydroxyphenyl)-γ-valerolactone]
M6	=	[5-(3′,4′,5′-trihydroxyphenyl)-γ-valerolactone]
NNK	=	4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
TPA	=	12-O-tetradecanoyl-13-acetate
DGT	=	decaffeinated green tea

Abbreviations:
EGCG	=	(−)-epigallocatechin gallate
ECG	=	(−)-epigallocatechin
EC	=	(−)-epicatechin
ECG	=	(−)-epicatechin gallate
M4	=	[5-(3′,4′-dihydroxyphenyl)-γ-valerolactone]
M6	=	[5-(3′,4′,5′-trihydroxyphenyl)-γ-valerolactone]
NNK	=	4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
TPA	=	12-O-tetradecanoyl-13-acetate
DGT	=	decaffeinated green tea