Power E G, Phillips I
Department of Microbiology, UMDS, St. Thomas' Hospital, London, UK.
FEMS Microbiol Lett. 1993 Sep 15;112(3):251-4. doi: 10.1111/j.1574-6968.1993.tb06458.x.
Quinolone antimicrobial agents induce the SOS response in bacteria, including the umuDC genes necessary for error-prone repair. Consequently these drugs may be mutagenic in bacteria with a functional SOS response. Differential killing tests with Escherichia coli WP2 (trp) and its repair-deficient derivative CM871 (trp lexA recA uvrA) indicated that a functional DNA repair system was protective against the action of quinolones, implying that quinolones are causing some form of DNA damage (not necessarily directly) and are therefore genotoxic. Dose-dependent reversion from His- to His+ with quinolones was observed in the Ames test with Salmonella typhimurium TA102 (uvr+) but in no other Salmonella tester strains (all uvr-), suggesting that a functional excision repair system is essential for quinolone-induced bacterial mutagenesis. A significant correlation between SOS inducing potential (SOSIP) and mutagenic potential in the Ames test (r = 0.89) indicated that quinolone-induced mutagenic effects in bacteria are almost entirely due to SOS-processed DNA damage.
喹诺酮类抗菌剂可诱导细菌中的SOS反应，包括易错修复所需的umuDC基因。因此，这些药物可能对具有功能性SOS反应的细菌具有致突变性。用大肠杆菌WP2（trp）及其修复缺陷衍生物CM871（trp lexA recA uvrA）进行的差异杀伤试验表明，功能性DNA修复系统可保护细菌免受喹诺酮类药物的作用，这意味着喹诺酮类药物正在造成某种形式的DNA损伤（不一定是直接损伤），因此具有基因毒性。在鼠伤寒沙门氏菌TA102（uvr+）的艾姆斯试验中观察到喹诺酮类药物使His-向His+发生剂量依赖性回复突变，但在其他沙门氏菌测试菌株（均为uvr-）中未观察到，这表明功能性切除修复系统对于喹诺酮类药物诱导的细菌诱变至关重要。SOS诱导潜力（SOSIP）与艾姆斯试验中的诱变潜力之间存在显著相关性（r = 0.89），表明喹诺酮类药物在细菌中诱导的诱变效应几乎完全归因于SOS处理的DNA损伤。
