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氧化应激的分子机制和生理后果:来自模式细菌的教训。

The molecular mechanisms and physiological consequences of oxidative stress: lessons from a model bacterium.

机构信息

Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA.

出版信息

Nat Rev Microbiol. 2013 Jul;11(7):443-54. doi: 10.1038/nrmicro3032. Epub 2013 May 28.

Abstract

Oxic environments are hazardous. Molecular oxygen adventitiously abstracts electrons from many redox enzymes, continuously forming intracellular superoxide and hydrogen peroxide. These species can destroy the activities of metalloenzymes and the integrity of DNA, forcing organisms to protect themselves with scavenging enzymes and repair systems. Nevertheless, elevated levels of oxidants quickly poison bacteria, and both microbial competitors and hostile eukaryotic hosts exploit this vulnerability by assaulting these bacteria with peroxides or superoxide-forming antibiotics. In response, bacteria activate elegant adaptive strategies. In this Review, I summarize our current knowledge of oxidative stress in Escherichia coli, the model organism for which our understanding of damage and defence is most well developed.

摘要

缺氧环境是有危险的。分子氧偶然从许多氧化还原酶中提取电子,不断形成细胞内超氧化物和过氧化氢。这些物质可以破坏金属酶的活性和 DNA 的完整性,迫使生物体用清除酶和修复系统来保护自己。然而,氧化剂水平的升高会迅速毒害细菌,微生物竞争者和敌对的真核宿主都会利用这一弱点,用过氧化物或形成超氧化物的抗生素攻击这些细菌。作为回应,细菌激活了精致的适应策略。在这篇综述中,我总结了我们目前对大肠杆菌中氧化应激的认识,大肠杆菌是我们对损伤和防御理解最成熟的模式生物。

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