1. Nine habitual tea-drinking volunteers were recruited and asked to follow a low-polyphenol and low-caffeine diet for 6 days and to provide daily 24-h urine samples. On day 4 of the experiment strong black tea brewed under standardized conditions was re-introduced to the volunteers' diet. 2. 1H-NMR and HPLC profiling of the urine samples indicated that consumption of black tea (6-10 mugs per day) was associated with a significant (p = 0.00017) increase in hippuric acid excretion relative to control, increasing from 153-512 to 742-1374 mg day(-1). The excretion of substantial amounts of hippuric acid has not previously been associated with black tea consumption. 3. For some volunteers, the quantity of benzoic acid processed exceeded the acceptable daily intake (ADI), but this is not considered to constitute any hazard. 4. A mass-balance analysis indicated that the necessary quantity of benzoic acid could not be obtained from the contents of gallic acid, flavanols, flavonol glycosides and theaflavins in black tea even if 100% transformation was obtained, suggesting that the thearubigins (the major and chemically ill-defined polyphenols of black tea) may be an important source.
Theafulvins were isolated from black tea aqueous infusions and their antimutagenic activity was evaluated against a number of food carcinogens. Theafulvins gave rise to a concentration-dependent inhibition of the mutagenicity of 2-amino-3-methylimidazo-[4,5-f]quinoline, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene, nitrosopyrrolidine and nitrosopiperidine, but, in contrast, the mutagenicity of aflatoxin B1 was enhanced. The mutagenicity exhibited by N'-methyl-N'-nitro-N-nitrosoguanidine and 9-aminoacridine was not influenced and weakly inhibited by theafulvins, respectively. The p-hydroxylation of aniline and the O-dealkylations of methoxy-, ethoxy- and, to a lesser extent, pentoxyresorufin were inhibited by theafulvins in a concentration-dependent manner. When microsomal metabolism was terminated after metabolic activation of the promutagens, incorporation of the theafulvins into the activation system did not modulate the mutagenic response. It is concluded that theafulvins play an important role in the antimutagenic activity of black tea by inhibiting cytochrome P450-dependent bioactivation of the carcinogens.
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