1,2 - 二溴乙烷对大肠杆菌致突变性的分析：DNA修复活性和代谢途径的影响
An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: influence of DNA repair activities and metabolic pathways.
作者信息
Foster P L, Wilkinson W G, Miller J K, Sullivan A D, Barnes W M
机构信息
Division of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, MA 02118.
出版信息
Mutat Res. 1988 Nov;194(3):171-81. doi: 10.1016/0167-8817(88)90019-3.
Abstract
The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.
摘要
1,2 - 二溴乙烷（EDB）对大肠杆菌的致突变性可被紫外线诱导的切除修复系统降低，但不受主要的脱嘌呤/脱嘧啶位点修复功能丧失的影响。在高剂量下，70 - 90%的EDB诱导的突变独立于SOS诱变过程，约50%独立于谷胱甘肽结合。EDB诱导的SOS非依赖性突变不受修复烷基化诱导的DNA损伤的酶的影响。EDB诱导的碱基替换以GC到AT和AT到GC的转换为主。这些结果表明，EDB诱导的前诱变损伤具有一些但并非全部简单烷基损伤的特征。
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