Bu-Abbas A, Clifford M N, Walker R, Ioannides C
Division of Toxicology, School of Biological Sciences, University of Surrey, Guildford, UK.
Mutagenesis. 1994 Jul;9(4):325-31. doi: 10.1093/mutage/9.4.325.
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)
在本研究中，对绿茶水提取物按照人类通常的饮用浓度进行评估，以考察其对主要类别膳食和职业致癌物的抗诱变活性。绿茶提取物对杂环胺（IQ和Glu-P-1）和多环芳烃（苯并[a]芘和7,12-二甲基苯并[a]蒽）经Aroclor 1254-肝S9介导的诱变性以及亚硝胺（亚硝基哌啶和亚硝基吡咯烷）经异烟肼诱导的S9介导的诱变性均产生了非常显著且浓度依赖性的抑制作用。对于两种芳香胺，即2-氨基芴和2-氨基蒽，无论以Aroclor 1254-S9、分离的微粒体还是胞液作为活化系统，其诱变性也出现了类似的抑制。最后，绿茶提取物对直接作用诱变剂9-氨基吖啶和MNNG的诱变性也有抑制作用，但与间接作用诱变剂相比，效果不那么明显。绿茶提取物使甲氧基试卤灵、乙氧基试卤灵和戊氧基试卤灵的O-脱烷基作用显著且呈浓度依赖性降低。还观察到对细胞色素c的NADPH依赖性还原有类似抑制作用。在各种前诱变剂的微粒体代谢终止后，将绿茶提取物加入活化系统会导致其诱变反应受到相对适度的抑制。得出的结论是，绿茶水提取物对多种重要的膳食和环境诱变剂具有显著的抗诱变潜力。似乎有两种机制起作用。第一种涉及各种前诱变剂的活性遗传毒性物质与水提取物中存在的亲核性茶叶成分之间的直接相互作用。（摘要截短于250词）
