Rats were exposed to freshly prepared aqueous extracts of green tea (2.5% w/v) as the sole source of drinking water for 4 weeks. Hepatic cytochrome P450 activity was determined using chemical probes, showing selectivity for particular isoforms, and by immunoblot analysis employing polyclonal antibodies. Exposure to green tea gave rise to increases in the O-demethylation of methoxyresorufin and, to a lesser extent, in the dealkylations of ethoxyresorufin and pentoxyresorufin. An increase was also seen in lauric acid hydroxylation but, in contrast, the N-demethylation of erythromycin was inhibited. p-Nitrophenol oxidase activity was unaffected by the same treatment. Immunoblot analysis revealed increases in the apoprotein levels of CYP1A2 and CYP4A1 following treatment with green tea. A significant increase was also noted in the CN(-)-insensitive palmitoyl CoA oxidation and this was paralleled by an increase in the levels of the peroxisomal trifunctional protein determined immunologically. Hepatic S9 and microsomal preparations from tea-treated animals were more effective than controls in activating 2-amino-3-methylimidazol[4,5-f]quinoline and 2-aminoanthracene to mutagens in the Ames test. When N-nitrosopyrrolidine served as the promutagen, tea did not influence its mutagenicity when isolated microsomes comprised the activation system but a significant inhibition was observed when hepatic S9 was used. The above findings are discussed within the context of the established anticarcinogenic and anti-mutagenic properties of green tea.
In the present study aqueous extracts of green tea, at the concentrations customarily consumed by humans, were evaluated for their antimutagenic activity against major classes of dietary and occupational carcinogens. Green tea extracts caused a very marked and concentration-dependent inhibition of the Aroclor 1254-hepatic S9-mediated mutagenicity of heterocyclic amines (IQ and Glu-P-1) and polycyclic aromatic hydrocarbons (benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene) and of the isoniazid-induced S9-mediated mutagenicity of nitrosamines (nitrosopiperidine and nitrosopyrrolidine). Similar inhibition was seen in the mutagenicity of the two aromatic amines, namely 2-amino-fluorene and 2-aminoanthracene, whether Aroclor 1254-S9, isolated microsomes or cytosol served as the activation system. Finally, the mutagenicity of the direct-acting mutagens 9-aminoacridine and MNNG was also suppressed by green tea extracts, but the effect was less pronounced when compared with the indirect-acting mutagens. Green tea extracts caused a marked and concentration-dependent decrease in the O-dealkylation of methoxyresorufin, ethoxyresorufin and pentoxyresorufin. A similar inhibition of the NADPH-dependent reduction of cytochrome c was also observed. Following the termination of the microsomal metabolism of the various promutagens, incorporation of green tea extracts into the activation system resulted in a comparatively modest inhibition of their mutagenic response. It is concluded that aqueous extracts of green tea possess marked antimutagenic potential against a variety of important dietary and environmental mutagens. Two mechanisms appear to be responsible. The first involves a direct interaction between the reactive genotoxic species of the various promutagens and nucleophilic tea component(s) present in the aqueous extracts.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study was undertaken to compare the antimutagenic activity of aqueous extracts, at the concentrations used for human consumption, from green, black and decaffeinated black tea. Antimutagenic potential was evaluated against three indirect-acting dietary carcinogens, Glu-P-1, benzo(a)pyrene and nitrosopyrrolidine. All three types of tea gave rise to strong and concentration-dependent suppression of the mutagenicity of the three premutagens in the presence of an activation system. No major difference in the antimutagenic potential of the three types of tea could be discerned. Black tea, decaffeinated black tea and, to a lesser extent, green tea also antagonized the mutagenicity of the direct-acting mutagen 9-aminoacridine. All three types of tea inhibited markedly the NADPH-dependent reduction of cytochrome c and the O-dealkylations of ethoxy-, methoxy- and, to a much lesser extent, pentoxy-resorufin. When the microsomal metabolism was terminated, after the metabolic activation of the premutagens, incorporation of the aqueous tea extracts into the activation system caused a concentration-dependent suppression of mutagenic response. No significant difference in the antimutagenic activity of the three types of tea in this system was evident. Bearing in mind the much higher concentration of flavanols in green tea compared with the black teas, it may be concluded either that these compounds are unlikely to be the major tea components responsible for the antimutagenic, and possibly anticarcinogenic, properties of tea or that their fermentation products are similarly active.
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