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黄曲霉毒素Q1在有或无大鼠或人肝微粒体制剂存在的情况下对鼠伤寒沙门氏菌TA 100的致突变性。

The mutagenicity of aflatoxin Q1 to Salmonella typhimurium TA 100 with or without rat or human liver microsomal preparations.

作者信息

Yourtee D M, Kirk-Yourtee C L

出版信息

Res Commun Chem Pathol Pharmacol. 1986 Oct;54(1):101-13.

PMID:3099349
Abstract

An investigation of the mutagenicity of aflatoxin Q1 in the Salmonella-mutagenicity test is reported. This mammalian metabolite of aflatoxin B1 was marginally mutagenic to strain TA 98 when either rat or human liver microsomes were present in the test. However, it was mutagenic to TA 100 with the same liver activation sources in the assay. Moreover, it was mutagenic to TA 100 in the absence of liver microsomes. This Q1 mutagenesis, presumably a direct acting base substitution effect, was nearly equal to the liver activated mutagenesis. It was also greater in this respect than aflatoxin B1 or aflatoxicol.

摘要

本文报道了黄曲霉毒素Q1在沙门氏菌致突变试验中致突变性的研究。黄曲霉毒素B1的这种哺乳动物代谢产物,在试验中存在大鼠或人肝微粒体时,对TA 98菌株有轻微的致突变性。然而,在该试验中,对于相同的肝激活源,它对TA 100有致突变性。此外,在没有肝微粒体的情况下,它对TA 100也有致突变性。这种Q1的致突变作用,推测是一种直接作用的碱基置换效应,几乎等同于肝激活的致突变作用。在这方面,它也比黄曲霉毒素B1或黄曲霉毒素醇更强。

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