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首页> 外文期刊>Biochimica et Biophysica Acta. General Subjects >Periplasmic Cu,Zn superoxide dismutase and cytoplasmic Dps concur in protecting Salmonella enterica serovar Typhimurium from extracellular reactive oxygen species
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Periplasmic Cu,Zn superoxide dismutase and cytoplasmic Dps concur in protecting Salmonella enterica serovar Typhimurium from extracellular reactive oxygen species

机译：周质铜，锌超氧化物歧化酶和细胞质Dps共同保护肠炎沙门氏菌血清鼠伤寒免受细胞外活性氧的影响

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Several bacteria possess periplasmic Cu,Zn superoxide dismutases which can confer protection from extracellular reactive oxygen species. Thus, deletion of the sodC1 gene reduces Salmonella enterica serovar Typhimurium ability to colonize the spleens of wild type mice, but enhances virulence in p47phox mutant mice. To look into the role of periplamic Cu,Zn superoxide dismutase and into possible additive effects of the ferritin-like Dps protein involved in hydrogen peroxide detoxification, we have analyzed bacterial survival in response to extracellular sources of superoxide and/or hydrogen peroxide. Exposure to extracellular superoxide of Salmonella Typhimurium mutant strains lacking the sodC1 and sodC2 genes and/or the dps gene does not cause direct killing of bacteria, indicating that extracellular superoxide is poorly bactericidal. In contrast, all mutant strains display a sharp hydrogen peroxide-dependent loss of viability, the dps,sodC1,sodC2 mutant being less resistant than the dps or the sodC1,sodC2 mutants. These findings suggest that the role of Cu,Zn superoxide dismutase in bacteria is to remove rapidly superoxide from the periplasm to prevent its reaction with other reactive molecules. Moreover, the nearly additive effect of the sodC and dps mutations suggests that localization of antioxidant enzymes in different cellular compartments is required for bacterial resistance to extracytoplasmic oxidative attack. (C) 2007 Elsevier B.V. All rights reserved.
机译：几种细菌具有周质的铜，锌超氧化物歧化酶，可以提供针对细胞外活性氧的保护。因此，sodC1基因的缺失降低了肠炎沙门氏菌鼠伤寒沙门氏菌定居野生型小鼠脾脏的能力，但增强了p47phox突变小鼠的毒性。为了研究周质性铜，锌超氧化物歧化酶的作用，以及参与过氧化氢解毒的铁蛋白样Dps蛋白可能产生的加成作用，我们分析了细菌对细胞外源超氧化物和/或过氧化氢的响应。缺少sodC1和sodC2基因和/或dps基因的鼠伤寒沙门氏菌突变株暴露于细胞外超氧化物不会导致细菌的直接杀灭，这表明细胞外超氧化物的杀菌性很差。相比之下，所有突变株均显示出过氧化氢依赖性的急剧降低的活力，dps，sodC1，sodC2突变体的抗药性低于dps或sodC1，sodC2突变体。这些发现表明，铜，锌超氧化物歧化酶在细菌中的作用是从周质中快速去除超氧化物，以防止其与其他反应性分子发生反应。此外，sodC和dps突变的几乎加和作用表明，细菌对细胞外质氧化攻击的抗性要求将抗氧化酶定位在不同的细胞区室中。 （C）2007 Elsevier B.V.保留所有权利。

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