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

被引:1108
|
作者
Imlay, James A. [1 ]
机构
[1] Univ Illinois, Dept Microbiol, Urbana, IL USA
关键词
ENDOGENOUS HYDROGEN-PEROXIDE; ESCHERICHIA-COLI RESPONSE; OXYR TRANSCRIPTION FACTOR; FE-S CLUSTER; SUPEROXIDE-DISMUTASE; DNA-DAMAGE; PSEUDOMONAS-AERUGINOSA; SALMONELLA-ENTERICA; FUMARATE REDUCTASE; PRIMARY TARGETS;
D O I
10.1038/nrmicro3032
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
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.
引用
收藏
页码:443 / 454
页数:12
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