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根据各种茶对2-氨基-3-甲基咪唑[4,5-f]喹啉和苯并[a]芘诱变作用的影响判断其抗诱变的可能机制。

Possible mechanisms of antimutagens by various teas as judged by their effects on mutagenesis by 2-amino-3-methylimidazo[4,5-f]quinoline and benzo[a]pyrene.

作者信息

Chen H Y, Yen G C

机构信息

Department of Food Science, National Chung Hsing University, Taichung, Taiwan, ROC.

出版信息

Mutat Res. 1997 Sep 18;393(1-2):115-22. doi: 10.1016/s1383-5718(97)00092-2.

Abstract

Possible mechanisms of antimutagenicity of various tea extracts (green, pouchong, oolong and black tea) toward 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and benzo[a]pyrene (B[a]P) were investigated using a Salmonella/microsome assay. Tea extracts exhibited no inhibitory effects toward IQ and B[a]P in bio-antimutagenic assays, indicating that their antimutagenic activity is desmutagenic in nature. The mutagenicities of IQ and B[a]P decreased as the reaction periods of tea extracts with promutagens, S9 mix, or mutagen metabolites increased. The antimutagenicity of tea extracts toward IQ could be attributed (primarily) to an interaction between tea extracts and S9 mix. Apart from their interaction with S9 mix, tea extracts also exhibited antimutagenicity by markedly decreasing the mutagenicity of B[a]P metabolites. These results suggest that tea extracts: (1) inhibit the cytochrome P-450-mediated metabolism of IQ and B[a]P to their ultimate mutagenic metabolite form; and (2) interact with both promutagens and their metabolites in such a way as to reduce their mutagenic potentials. Therefore, the antimutagenic actions of tea extracts are due to a combination of the above distinctive mechanisms, and can vary with the type of mutagen under test.

摘要

利用沙门氏菌/微粒体试验,研究了各种茶提取物(绿茶、包种茶、乌龙茶和红茶)对2-氨基-3-甲基咪唑[4,5-f]喹啉(IQ)和苯并[a]芘(B[a]P)的抗诱变可能机制。在生物抗诱变试验中,茶提取物对IQ和B[a]P没有抑制作用,表明它们的抗诱变活性本质上是去诱变的。随着茶提取物与前诱变剂、S9混合物或诱变代谢物的反应时间增加,IQ和B[a]P的诱变性降低。茶提取物对IQ的抗诱变作用(主要)可归因于茶提取物与S9混合物之间的相互作用。除了与S9混合物相互作用外,茶提取物还通过显著降低B[a]P代谢物的诱变性而表现出抗诱变作用。这些结果表明,茶提取物:(1)抑制细胞色素P-450介导的IQ和B[a]P代谢为其最终诱变代谢物形式;(2)与前诱变剂及其代谢物相互作用,从而降低它们的诱变潜力。因此,茶提取物的抗诱变作用是上述独特机制共同作用的结果,并且可能因受试诱变剂类型而异。

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