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杀螟硫磷在细菌和哺乳动物细胞中的致突变性研究。

Mutagenicity studies on fenitrothion in bacteria and mammalian cells.

作者信息

Hara M, Kogiso S, Yamada F, Kawamoto M, Yoshitake A, Miyamoto J

机构信息

Laboratory of Biochemistry and Toxicology, Sumitomo Chemical Co., Ltd., Osaka, Japan.

出版信息

Mutat Res. 1989 Jan;222(1):53-61. doi: 10.1016/0165-1218(89)90035-9.

Abstract

The mutagenicity of fenitrothion was determined in strains of Salmonella typhimurium and Escherichia coli. Fenitrothion was found to be non-mutagenic in Salmonella typhimurium strains of TA98, TA1535 and TA1537 and in Escherichia coli WP2uvrA both with and without S9 mix, while weak mutagenicity was observed only in Salmonella typhimurium TA100 and enhanced by the addition of S9 mix. The mutagenicity observed in the TA100 strain was not expressed in a nitroreductase-deficient strain, TA100 NR, and decreased in a transacetylase-deficient strain, TA100 1,8-DNP6. The mutagenicity of fenitrothion was also examined by a gene mutation assay using the gene for hypoxanthine-guanine phosphoribosyltransferase (hgprt) in V79 Chinese hamster lung cells. Fenitrothion did not induce any increment of 6-thioguanine-resistant mutant cells at doses ranging from 0.01 to 0.3 mM regardless of the presence or absence of S9 mix. These results suggest that reduction of fenitrothion by a bacterial nitroreductase of TA100 to an active form is essential for the expression of the mutagenicity of fenitrothion in TA100 and that a bacterial transacetylase of TA100 also has an important role in the process of mutagenic activation.

摘要

对硫磷的致突变性在鼠伤寒沙门氏菌和大肠杆菌菌株中进行了测定。结果发现,对硫磷在TA98、TA1535和TA1537鼠伤寒沙门氏菌菌株以及大肠杆菌WP2uvrA中,无论有无S9混合物存在,均无致突变性;而仅在鼠伤寒沙门氏菌TA100中观察到弱致突变性,且添加S9混合物后致突变性增强。在TA100菌株中观察到的致突变性在硝基还原酶缺陷菌株TA100 NR中未表现出来,而在转乙酰酶缺陷菌株TA100 1,8 - DNP6中致突变性降低。还通过使用V79中国仓鼠肺细胞中的次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶(hgprt)基因的基因突变试验检测了对硫磷的致突变性。无论有无S9混合物,在0.01至0.3 mM的剂量范围内,对硫磷均未诱导6 - 硫鸟嘌呤抗性突变细胞增加。这些结果表明,TA100的细菌硝基还原酶将对硫磷还原为活性形式对于对硫磷在TA100中的致突变性表达至关重要,并且TA100的细菌转乙酰酶在诱变活化过程中也起重要作用。

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