环氧乙烷在大肠杆菌中诱导的不依赖recA的致突变性。
recA-independent mutagenicity induced by chloroethylene oxide in E. coli.
作者信息
Barbin A, Tenenbaum L, Toman Z, Radman M, Bartsch H
出版信息
Mutat Res. 1985 Nov-Dec;152(2-3):157-9. doi: 10.1016/0027-5107(85)90057-0.
The mechanism of mutagenicity of chloroethylene oxide (CEO), an ultimate carcinogenic metabolite of vinyl chloride, was investigated in 3 Escherichia coli strains (E. coli "multitest"). In this system, the mutagenicity of CEO was found to be mainly SOS-independent. CEO did not induce recombinational events at a detection level of about 10(-2) recombinants/survivor. Our results indicate that CEO- (or vinyl chloride-) induced bacterial mutagenesis arises mainly from miscoding DNA adducts.
对氯乙烯的最终致癌代谢产物氯代环氧乙烷（CEO）的致突变机制，在3种大肠杆菌菌株（大肠杆菌“多重测试”）中进行了研究。在该系统中，发现CEO的致突变性主要不依赖于SOS。在约10^(-2)个重组体/存活菌的检测水平下，CEO未诱导重组事件。我们的结果表明，CEO（或氯乙烯）诱导的细菌突变主要源于错配DNA加合物。
Zotero 插件