Molecular Mechansims for Cellular Responses to Radiation and Oxidative Stresses

我们研究了硫氧还蛋白和硫氧还蛋白还原酶保护大肠杆菌细胞对抗过氧化氢的途径。在固定阶段，硫氧还蛋白的还原形式通过清除活性氧来保护细胞。另一方面，在生长早期，硫氧还蛋白的氧化形式作为一种调节因子，用于诱导编码过氧化氢酶-过氧化物酶i的适应性反应基因，如katG，这些硫氧还蛋白系统的作用是由OxyR蛋白介导的。此外，在厌氧条件下，二胺诱导了katG基因的表达，这表明氧化还原平衡的破坏导致了在没有过氧化氢的情况下诱导了OxyR调控。因此，硫氧还蛋白的氧化还原状态是大肠杆菌氧化还原应激反应的关键因素。我们检测了硫氧还蛋白和硫氧还蛋白还原酶的表达调控。

We examined the pathways that thioredoxin and thioredoxin reductase protect Escherichia coli cells against hydrogen peroxide. In stationary phase, the reduced form of thioredoxin protected cells by scavenging reactive oxygen species. On the other hand, in early growth phase, the oxidized form of thioredoxin exerted as a regulatory factor for theinduction of adaptive response genes such as katG that encodes catalase- hydroperoxidase I.These effects of thioredoxin systems were mediated by the OxyR protein. In addition, the expression of the katG gene was induced by diamide under anaerobic conditions, suggesting that a disruption of redox balance results in the induction of OxyR regulon without hydrogen peroxide. Therefore, the redox state of thioredoxin is a critical factor for the redox stress response in E.coli. We examined the regulation of thioredoxin and thioredoxin reductase expression.