Abstract
Rats were maintained on aqueous extracts (2.5%, w/v) of green tea, black tea, and decaffeinated black tea, and after 4 weeks, received a single, oral dose of the food carcinogen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). Urine was collected for 48 h, and the excretion of urinary mutagens determined. Consumption of green tea and black tea, but not of decaffeinated black tea, markedly decreased the excretion of urinary mutagens and promutagens. In a further study, supplementing decaffeinated black tea with caffeine also suppressed the urinary excretion of mutagenic material in rats treated with IQ. Rats were maintained on similar preparations of tea for 4 weeks and hepatic and extrahepatic DNA adduct formation determined 16 h after administration of a single, oral dose of IQ, utilising the 32P-postlabelling-HPLC assay. Decaffeinated black tea caused a statistically-significant increase in hepatic IQ-DNA adduct formation. Rats were maintained on similar aqueous extracts (2.5%, w/v) of tea or on a solution of caffeine of similar concentration to that found in black tea (700 mg I -1) for 4 weeks. Two further groups of animals were administered solutions of black tea theaflavins or theafulvins for 4 weeks. Determination of intestinal phase I and II xenobiotic-metabolising enzyme activities and immunoblot analyses failed to reveal any significant differences between any of the treatments and the control. Green tea (2.5%, w/v) was fractionated by HPLC and the fractions evaluated for antimutagenic potential. One fraction, that corresponding to (-)-epigallocatechin gallate (EGCG), exhibited the greatest suppression of IQ-induced mutagenicity, primarily by inhibiting the bioactivation of the mutagen. Inhibition of methoxyresorufin O-demethylase by the fraction, used as a marker for CYP1A2 activity, was abolished following treatment with degallase. It is concluded that tea modulates the metabolism of IQ, and that the antigenotoxic effect of tea is mediated largely by caffeine and EGCG.