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酚类化合物抑制N-甲基-N'-硝基-N-亚硝基胍诱导诱变的机制。

Mechanism of inhibition of N-methyl-N'-nitro-N-nitrosoguanidine-induced mutagenesis by phenolic compounds.

作者信息

Chan R I, San R H, Stich H F

出版信息

Cancer Lett. 1986 Apr;31(1):27-34. doi: 10.1016/0304-3835(86)90163-1.

Abstract

At non-toxic concentrations, 2 naturally occurring phenolic compounds, caffeic acid and chlorogenic acid, suppressed the mutagenic activity of the carcinogen N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Salmonella typhimurium strain TA1535. The inhibitory effect was observed only when the phenolic compound and the mutagen were administered concurrently. The interaction between phenolic compounds and MNNG was also studied in a cell-free system using a colorimetric method. The results are consistent with the assumption that phenolic compounds scavenge reactive electrophilic MNNG degradation products, thereby preventing their action on critical cellular targets.

摘要

在无毒浓度下,两种天然存在的酚类化合物,咖啡酸和绿原酸,抑制了致癌物N-甲基-N'-硝基-N-亚硝基胍(MNNG)在鼠伤寒沙门氏菌TA1535菌株中的致突变活性。仅当酚类化合物和诱变剂同时给药时才观察到抑制作用。还使用比色法在无细胞系统中研究了酚类化合物与MNNG之间的相互作用。结果与以下假设一致,即酚类化合物清除反应性亲电MNNG降解产物,从而防止它们对关键细胞靶点的作用。

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