Aiming to clarify the mechanisms by which eukaryotes acquire tolerance to oxidative stress, adaptive and cross-protection responses to oxidants were investigated in Saccharomyces cerevisiae. Cells treated with sub-lethal concentrations of menadione (a source of superoxide anions) exhibited cross-protection against lethal doses of peroxide; however, cells treated with H2O2 did not acquire tolerance to a menadione stress, indicating that menadione response encompasses H2O2 adaptation. Although, deficiency in cytoplasmic superoxide dismutase (Sod1) had not interfered with response to superoxide, cells deficient in glutathione (GSH) synthesis were not able to acquire tolerance to H2O2 when pretreated with menadione. These results suggest that GSH is an inducible part of the superoxide adaptive stress response, which correlates with a decrease in the levels of intracellular oxidation. On the other hand, neither the deficiency of Sod1 nor in GSH impaired the process of acquisition of tolerance to H2O2 achieved by a mild pretreatment with peroxide. Using a strain deficient in the cytosolic catalase, we were able to conclude that the reduction in lipid peroxidation levels produced by the adaptive treatment with H2O2 was dependent on this enzyme. Corroborating these results, the pretreatment with low concentrations of H2O2 promoted an increase in catalase activity.

中文翻译：

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真核生物中的氧化应激反应：谷胱甘肽，超氧化物歧化酶和过氧化氢酶对酿酒酵母中过氧化物和甲萘醌应力适应的影响。

为了阐明真核生物获得对氧化应激的耐受性的机制，在酿酒酵母中研究了对氧化剂的适应性和交叉保护反应。用亚致死浓度的甲萘醌（超氧化物阴离子源）处理的细胞对致命剂量的过氧化物具有交叉保护作用。然而，用H2O2处理的细胞未获得对甲萘醌应力的耐受性，表明甲萘醌反应包括H2O2适应性。尽管细胞质超氧化物歧化酶（Sod1）的缺乏并未干扰对超氧化物的反应，但是在用甲萘醌预处理时，缺乏谷胱甘肽（GSH）合成的细胞无法获得对H2O2的耐受性。这些结果表明，谷胱甘肽过氧化物酶是超氧化物适应应激反应的可诱导部分，这与细胞内氧化水平的降低有关。另一方面，Sod1和GSH的缺乏都不会损害通过过氧化物温和预处理实现的对H2O2耐受性的获得过程。使用缺乏胞质过氧化氢酶的菌株，我们能够得出结论，H2O2适应性处理产生的脂质过氧化水平的降低取决于该酶。证实了这些结果，用低浓度的H2O2进行预处理可促进过氧化氢酶活性的提高。我们能够得出结论，H2O2适应性处理所产生的脂质过氧化水平的降低取决于该酶。证实了这些结果，用低浓度的H2O2进行预处理可促进过氧化氢酶活性的提高。我们能够得出结论，H2O2适应性处理所产生的脂质过氧化水平的降低取决于该酶。证实了这些结果，用低浓度的H2O2进行预处理可促进过氧化氢酶活性的提高。