Zhang Q M, Takemoto T, Mito S, Yonei S
Laboratory of Radiation Biology, Graduate School of Science, Kyoto University, Japan.
J Radiat Res. 1996 Sep;37(3):171-6. doi: 10.1269/jrr.37.171.
We examined whether or not peroxide stress induces a repair capacity for oxidatively damaged DNA in Escherichia coli cells. Peroxide stress was brought about by adding 30 microM hydrogen peroxide (H2O2) to exponentially growing cells. The following results were obtained. (1) After exposure to H2O2, E. coli resistance to X-rays was enhanced. The acquisition of resistance was inhibited by rifampicin and chloramphenicol. (2) The response was acquired in mutants defective in the katG and oxyR genes, as well as in the wild-type strain. (3) Lambda phages damaged by exposure to H2O2 showed higher survival on H2O2-treated cells than on untreated cells. (4) The peroxide stress did not render E. coli cells resistant to UV and mitomycin C. These suggest that peroxide stress induces a repair capacity against oxidative DNA damage and that this response must be regulated by a different mechanism from oxyR(+)-mediated regulatory system.
我们研究了过氧化物胁迫是否会诱导大肠杆菌细胞对氧化损伤DNA的修复能力。通过向指数生长期的细胞中添加30微摩尔过氧化氢(H2O2)来产生过氧化物胁迫。得到了以下结果。(1)暴露于H2O2后,大肠杆菌对X射线的抗性增强。利福平和平氯霉素可抑制抗性的获得。(2)在katG和oxyR基因缺陷的突变体以及野生型菌株中都获得了这种反应。(3)暴露于H2O2而受损的λ噬菌体在H2O2处理过的细胞上比在未处理的细胞上具有更高的存活率。(4)过氧化物胁迫并未使大肠杆菌细胞对紫外线和丝裂霉素C产生抗性。这些结果表明,过氧化物胁迫诱导了针对氧化性DNA损伤的修复能力,并且这种反应一定是由一种不同于oxyR(+)介导的调节系统的机制所调节的。