Document Detail


The redox stress hypothesis of aging.
MedLine Citation:
PMID:  22080087     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The main objective of this review is to examine the role of endogenous reactive oxygen/nitrogen species (ROS) in the aging process. Until relatively recently, ROS were considered to be potentially toxic by-products of aerobic metabolism, which, if not eliminated, may inflict structural damage on various macromolecules. Accrual of such damage over time was postulated to be responsible for the physiological deterioration in the postreproductive phase of life and eventually the death of the organism. This "structural damage-based oxidative stress" hypothesis has received support from the age-associated increases in the rate of ROS production and the steady-state amounts of oxidized macromolecules; however, there are increasing indications that structural damage alone is insufficient to satisfactorily explain the age-associated functional losses. The level of oxidative damage accrued during aging often does not match the magnitude of functional losses. Although experimental augmentation of antioxidant defenses tends to enhance resistance to induced oxidative stress, such manipulations are generally ineffective in the extension of life span of long-lived strains of animals. More recently, in a major conceptual shift, ROS have been found to be physiologically vital for signal transduction, gene regulation, and redox regulation, among others, implying that their complete elimination would be harmful. An alternative notion, advocated here, termed the "redox stress hypothesis," proposes that aging-associated functional losses are primarily caused by a progressive pro-oxidizing shift in the redox state of the cells, which leads to the overoxidation of redox-sensitive protein thiols and the consequent disruption of the redox-regulated signaling mechanisms.
Authors:
Rajindar S Sohal; William C Orr
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-10-24
Journal Detail:
Title:  Free radical biology & medicine     Volume:  52     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-27     Completed Date:  2012-05-17     Revised Date:  2014-09-09    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  539-55     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Aging*
Animals
Cell Differentiation
Growth and Development
Humans
Oxidation-Reduction
Oxidative Stress*
Oxygen Consumption
Reactive Nitrogen Species / metabolism
Reactive Oxygen Species / metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
R01 AG007657/AG/NIA NIH HHS; R01 AG007657-23/AG/NIA NIH HHS; R01 AG013563/AG/NIA NIH HHS; R01 AG013563-13/AG/NIA NIH HHS; R01 AG017077/AG/NIA NIH HHS; R01 AG017077-05/AG/NIA NIH HHS; R01 AG13563/AG/NIA NIH HHS; R01 AG15122/AG/NIA NIH HHS; R01 AG17077/AG/NIA NIH HHS; R01 AG17526/AG/NIA NIH HHS; R01 AG20715/AG/NIA NIH HHS; R01 AG7657/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Nitrogen Species; 0/Reactive Oxygen Species
Comments/Corrections

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