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Curr Biol. 2014 May 19;24(10):R453-62. doi: 10.1016/j.cub.2014.03.034.

ROS function in redox signaling and oxidative stress.

Author information

1
Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
2
Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: nav@northwestern.edu.

Abstract

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.

PMID:
24845678
PMCID:
PMC4055301
DOI:
10.1016/j.cub.2014.03.034
[Indexed for MEDLINE]
Free PMC Article

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