Todd M L, Schendel P F
J Bacteriol. 1983 Oct;156(1):6-12. doi: 10.1128/jb.156.1.6-12.1983.
The mutagenic and toxic effects of a series of N-alkyl-N'-nitro-N-nitrosoguanidines were examined in Escherichia coli K-12. The role of nucleotide excision repair, the SOS response, and the adaptive response in both the reduction and the production of the biological effects of these chemicals was tested. The effects of ethyl-nitrosoguanidine are similar in nucleotide excision repair-proficient and -deficient strains, but both the mutagenicity and the toxicity of alkyl groups larger than two carbons are significantly reduced by the presence of this repair system. Similarly, when alkyl groups are larger than two carbons, the umuC gene product is essential for the production of a fraction of the mutations that these lesions produce. The induction of the adaptive response had a significant effect on the toxicity of all of the chemicals tested, but its effect on mutagenicity was less uniform, having a larger effect on ethylating and propylating agents than on butylating and amylating agents.
在大肠杆菌K-12中检测了一系列N-烷基-N'-硝基-N-亚硝基胍的致突变和毒性作用。测试了核苷酸切除修复、SOS反应和适应性反应在降低和产生这些化学物质生物学效应中的作用。亚硝基胍在核苷酸切除修复 proficient和deficient菌株中的作用相似,但存在这种修复系统时,大于两个碳的烷基的致突变性和毒性均显著降低。同样,当烷基大于两个碳时,umuC基因产物对于这些损伤产生的一部分突变的产生至关重要。适应性反应的诱导对所有测试化学物质的毒性有显著影响,但其对致突变性的影响不太一致,对乙基化和丙基化剂的影响比对丁基化和戊基化剂的影响更大。