Murphey-Corb M, Kong H L, Murray M L
J Bacteriol. 1980 Apr;142(1):191-5. doi: 10.1128/jb.142.1.191-195.1980.
It has been observed previously that the mutagenic action of nitrous acid may be potentiated by polyamines. We examined the cellular response of two deoxyribonucleic acid repair systems to treatment with spermidine-nitrite reaction products. uvrB- deficient mutants of Salmonella typhimurium LT2 showed enhanced lethal and mutagenic response to the reaction products. Lethal activity was further enhanced in a uvrB recA double mutant, whereas mutagenic activity was not detectable. Dependence of mutagenesis on the recA gene implicates the action of an error-prone repair system in the fixation of a premutagenic lesion as a mutation. From consideration of the substrate characteristics of the two repair systems studied, it is suggested that the deoxyribonucleic acid lesion formed by the reaction products of spermidine and nitrite is an intrastrand cross-link.
以前已经观察到,亚硝酸的诱变作用可能会被多胺增强。我们研究了两个脱氧核糖核酸修复系统对亚精胺-亚硝酸盐反应产物处理的细胞反应。鼠伤寒沙门氏菌LT2的uvrB缺陷型突变体对反应产物表现出增强的致死和诱变反应。uvrB recA双突变体中的致死活性进一步增强,而诱变活性无法检测到。诱变对recA基因的依赖性表明,易错修复系统在将前诱变损伤固定为突变的过程中发挥了作用。从所研究的两个修复系统的底物特性来看,推测亚精胺和亚硝酸盐反应产物形成的脱氧核糖核酸损伤是链内交联。