ICR化合物的代谢失活与其在细菌和培养的哺乳动物细胞中的诱变差异之间的关系。

Relationships between metabolic deactivation of ICR compounds and their differential mutagenicity in bacteria and cultured mammalian cells.

作者信息

De Flora S, Basso C, Camoirano A, Astengo M, Badolati G S

出版信息

Mutat Res. 1986 Jul;174(3):227-32. doi: 10.1016/0165-7992(86)90156-9.

Abstract

Preparations of Chinese hamster ovary (CHO) cells decreased the genotoxicity of 3 ICR compounds (ICR 191, ICR 191-OH and ICR 170-OH), while they did not affect the genotoxicity of ICR 170 in the Salmonella reversion test nor in a DNA-repair test in E. coli. These data may contribute towards the explanation of the lack of activity of the two hydroxylated compounds in the CHO/HGPRT forward mutation system, as well as the different rank of mutagenicity of the two chloroethyl compounds in bacteria (ICR 191 greater than ICR 170), compared to cultured mammalian cells and in general to eukaryotic cells (ICR 170 greater than ICR 191).

摘要

中国仓鼠卵巢（CHO）细胞制剂降低了3种ICR化合物（ICR 191、ICR 191-OH和ICR 170-OH）的遗传毒性，而在沙门氏菌回复突变试验和大肠杆菌DNA修复试验中，它们对ICR 170的遗传毒性没有影响。这些数据可能有助于解释两种羟基化化合物在CHO/HGPRT正向突变系统中缺乏活性的原因，以及与培养的哺乳动物细胞和一般真核细胞相比，两种氯乙基化合物在细菌中的致突变性不同等级（ICR 191大于ICR 170），而在培养的哺乳动物细胞和一般真核细胞中（ICR 170大于ICR 191）。