ROS Function in Redox Signaling and Oxidative Stress

被引:4957
作者
Schieber, Michael [1 ]
Chandel, Navdeep S. [1 ]
机构
[1] Northwestern Univ, Div Pulm & Crit Care Med, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA
关键词
T-CELL-ACTIVATION; PROTEIN-TYROSINE PHOSPHATASES; MITOCHONDRIAL COMPLEX-III; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; CHRONOLOGICAL LIFE-SPAN; MN SUPEROXIDE-DISMUTASE; TUMOR-SUPPRESSOR PTEN; HYDROGEN-PEROXIDE; REVERSIBLE INACTIVATION; IMMUNE-RESPONSE;
D O I
10.1016/j.cub.2014.03.034
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) that cause damage to lipids, proteins and DNA. Oxidative stress has been linked to a myriad of pathologies. However, elevated ROS also act as signaling molecules in the maintenance of physiological functions a process termed redox biology. In this review we discuss the two faces of ROS redox biology and oxidative stress and their contribution to both physiological and pathological conditions. Redox biology involves a small increase in ROS levels that activates signaling pathways to initiate biological processes, while oxidative stress denotes high levels of ROS that result in damage to DNA, protein or lipids. Thus, the response to ROS displays hormesis, given that the opposite effect is observed at low levels compared with that seen at high levels. Here, we argue that redox biology, rather than oxidative stress, underlies physiological and pathological conditions.
引用
收藏
页码:R453 / R462
页数:10
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