Walters R N, Piddock L J, Wise R
Department of Medical Microbiology, Medical School, University of Birmingham, UK.
J Antimicrob Chemother. 1989 Dec;24(6):863-73. doi: 10.1093/jac/24.6.863.
The SOS response is induced in Escherichia coli by agents that damage DNA, such as quinolone antibiotics. It has been proposed that induction of the SOS response by these agents may have a role in the mechanism of quinolone action. SOS mutants derived from Escherichia coli AB1157 were investigated by susceptibility testing and killing kinetic studies at various quinolone concentrations to determine whether SOS response induction was protective or damaging to quinolone-treated bacteria. Susceptibility testing showed some differences between the SOS mutants, but killing kinetic studies demonstrated further differences, some of which could be explained with respect to the SOS phenotype. The effect of ciprofloxacin and nalidixic acid on the mutants cannot be explained with respect to the SOS phenotype, although the presence of a defective SOS response makes the bacteria less sensitive to the action of these agents. Evidence is provided that the induction of the SOS response may be protective to fleroxacin and enoxacin treated bacteria. These results suggest that quinolones may not have a common mechanism of action, as was first thought.
诸如喹诺酮类抗生素等能损伤DNA的药物可在大肠杆菌中诱导SOS应答。有人提出，这些药物诱导SOS应答可能在喹诺酮作用机制中发挥作用。通过在不同喹诺酮浓度下进行药敏试验和杀菌动力学研究，对源自大肠杆菌AB1157的SOS突变体进行了研究，以确定诱导SOS应答对喹诺酮处理的细菌是具有保护作用还是损害作用。药敏试验显示SOS突变体之间存在一些差异，但杀菌动力学研究表明了进一步的差异，其中一些差异可以根据SOS表型来解释。尽管存在缺陷的SOS应答会使细菌对这些药物的作用不太敏感，但环丙沙星和萘啶酸对突变体的影响无法根据SOS表型来解释。有证据表明，诱导SOS应答可能对氟罗沙星和依诺沙星处理的细菌具有保护作用。这些结果表明，喹诺酮类药物可能没有如最初所认为的那样的共同作用机制。
