Page J E, Ross H L, Bigger C A, Dipple A
Chemistry of Carcinogenesis Laboratory, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, MD 21702, USA.
Carcinogenesis. 1996 Feb;17(2):283-8. doi: 10.1093/carcin/17.2.283.
Mutation induction in the supF gene of the plasmid pS189 by 7-bromomethylbenz[a]anthracene and 7-bromomethyl-12-methylbenz[a]anthracene was examined. The former compound was substantially more mutagenic than the latter but a much greater proportion of the total mutations were located at mutation hotspots for the 12-methyl derivative. The overall correlation between sites of mutation and sites of polymerase arrest (an indicator of adduct formation) through the supF gene was poor. Although these bromocompounds should form only a single guanine adduct (unlike dihydrodiol epoxides that form both cis and trans adducts) more than one mutational change was found at a given site, although the predominant base substitution was G-->T for either compound.
研究了7-溴甲基苯并[a]蒽和7-溴甲基-12-甲基苯并[a]蒽对质粒pS189的supF基因的诱变作用。前一种化合物的诱变性明显高于后一种,但在总突变中,有更大比例的突变位于12-甲基衍生物的突变热点处。通过supF基因,突变位点与聚合酶停滞位点(加合物形成的一个指标)之间的总体相关性较差。尽管这些溴化合物应该只形成单一的鸟嘌呤加合物(与形成顺式和反式加合物的二氢二醇环氧化物不同),但在给定位点发现了不止一种突变变化,尽管两种化合物的主要碱基替换都是G→T。