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首页> 外文期刊>Fungal Biology Reviews >Oxidative stress response and adaptation to H2O2 in the model eukaryote Saccharomyces cerevisiae and its human pathogenic relatives Candida albicans and Candida glabrata
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Oxidative stress response and adaptation to H2O2 in the model eukaryote Saccharomyces cerevisiae and its human pathogenic relatives Candida albicans and Candida glabrata

机译：真核生物酿酒酵母及其人类致病亲属白色念珠菌和光滑念珠菌的氧化应激反应及对H2O2的适应

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Partial reduction of oxygen to water produces the reactive oxygen species hydrogen peroxide. This non-radical may leak from the respiratory chain in anaerobic cells or suddenly be generated during the 'respiratory burst' in phagocytic cells, which employ it as a first-line defense in response to microbial invaders. Excess hydrogen peroxide disturbs the cell's redox homeostasis and causes oxidative stress, thus demanding fine-tuned adaptive and protective mechanisms. The eukaryotic response to oxidative stress has been extensively studied in the model organism Saccharomyces cerevisiae whose considerable genetic toolbox facilitates comprehensive functional and systematic analyses. Depending on the severity of the oxidative onslaught, S. cerevisiae mounts distinct transcriptional response programs, which lead to adaptation or protection and eventually restoration of the redox homeostasis. This benign yeast is related to the two leading fungal pathogens of humans, Candida albicans and Candida glabrata. Both can cause life-threatening systemic infections but are precluded from traditional genetic analyses due to absence of meiosis. Yet, understanding how pathogens cope with oxidative stress is crucial to our understanding of virulence since oxidative stress is part of the innate immune response. This review summarizes the current state of our knowledge regarding the eukaryotic oxidative stress response in the context of adaptation and damage control based on insights gleaned in S. cerevisiae. Given the importance of oxidative defense, findings in the model system are compared to those obtained in both Candida pathogens where contributions to virulence are discussed. (C) 2015 The British Mycological Society. Published by Elsevier Ltd. All rights reserved.
机译：将氧气部分还原为水会产生活性氧过氧化氢。这种非自由基可能会从厌氧细胞的呼吸链中泄漏，或者在吞噬细胞的“呼吸爆发”期间突然产生，然后将其用作对微生物入侵者的一线防御。过量的过氧化氢干扰细胞的氧化还原稳态，并引起氧化应激，因此需要微调的适应性和保护性机制。真核生物对氧化应激的反应已在模型生物酿酒酵母中进行了广泛的研究，酿酒酵母具有大量的遗传工具，有助于进行全面的功能和系统分析。根据氧化攻击的严重程度，酿酒酵母安装不同的转录反应程序，从而导致适应性或保护性，并最终恢复氧化还原稳态。这种良性酵母与人类的两种主要真菌病原体白念珠菌和光滑念珠菌有关。两者均可导致威胁生命的全身感染，但由于缺乏减数分裂，因此无法进行传统的基因分析。然而，了解病原体如何应对氧化应激对我们对毒力的理解至关重要，因为氧化应激是先天免疫反应的一部分。这篇综述基于在酿酒酵母中获得的见解总结了我们在适应和损害控制的背景下有关真核生物氧化应激反应的知识的现状。考虑到氧化防御的重要性，将模型系统中的发现与两种念珠菌病原体中获得的毒力进行了比较。 （C）2015英国Mycological Society。由Elsevier Ltd.出版。保留所有权利。

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