oxyR基因对氧化物诱导SOS反应及SOD的影响

Effects of oxyR gene on SOS response and SOD induced by oxidants

本研究采用大肠杆菌ＰＱ６６及其ｏｘｙＲ基因缺失突变体ｏＧ４００作为生物指示体，观察到过氧化氢（Ｈ２Ｏ２）、异丁基过氧化氢（ＢＨＰ）、异丙基苯过氧化氢（ＣＨＰ）诱导ＯＧ４００、ＳＯＳ反应的敏感性明显高于ＰＱ６６，而甲醛（ＦＡ）及联二－Ｎ－甲基吡啶（ＭＶ）诱导的ＳＯＳ反应在两菌种间无差异，同时发现ＭＶ能诱导ＰＱ６６和ＯＧ４００超氧化物歧化酶（ＳＯＤ）的产生，且两菌种之间的诱导水平无差异，而Ｈ２Ｏ２不能诱导ＳＯＤ的产生。结果提示：ｏｘｙＲ基因的功能主要在于拮抗过氧化物引起的氧化损伤，对超氧化物诱导ＳＯＤ产生则无调节作用。

E.coli strains PQ66 and its oxyR deletion mutant OG400 were used as bioindicators in this study.It was observed that the sensitivity of SOS-induction by H2O2(peroxide hydrogen)、BHP(t-butyl hydroperoxide) or CHP(cumene hydroperoxide) in OG400 was much higher than that in PQ66,but the SOS response induced by MV(methyl viologen) or FA(formalin) had no diffirence between two strains.In addition,it was found that SOD(superoxide dismutase) activity could not be induced by H2O2 in PQ66,but by MV in PQ 66or OG400,and between two strains induced SOD levels were not diffirent.The results indicated that oxyR gene acted as the premier role against the oxidative damage by peroxides,but didn't regulate SOD-induction by superoxides.