Cited by 473Redox biology and oxidative stressGenetics, Aging, and Longevity in Model OrganismsAntioxidant Activity and Oxidative Stress

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The redox stress hypothesis of aging

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Sohal, Rajindar S., Orr, William C.·2012·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2011.10.445PMC PMC3267846

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Abstract

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.

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Authors: Sohal, R. S., & Orr, W. C.
Affiliations: University of Southern California (US)
Southern Methodist University (US)
Corresponding author: Sohal, Rajindar S.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2012-02
Volume: 52
Issue: 3
Pages: 539-555
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2011.10.445
PMC: PMC3267846
OpenAlex: W1986589519
Cited by: 473
References: 244
Citations by year: 2026: 14 · 2025: 22 · 2024: 21 · 2023: 24 · 2022: 24 · 2021: 24 · 2020: 29 · 2019: 32 · 2018: 34 · 2017: 35 · 2016: 33 · 2015: 46 · 2014: 57 · 2013: 43 · 2012: 32
FWCI: 3.83
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (R01 AG15122, R01 AG 17077, R01 AG13563, R01-AG 7657, R01 AG17526, R01AG020715, R01AG007657, R01AG013563, R01 AG20715, R01AG017526, R01AG015122, R01AG017077)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords: aging, reactive oxygen species, reactive nitrogen species, oxidative stress, redox regulation, protein thiol oxidation, antioxidant defense, lifespan extension, redox signaling
MeSH terms: Aging, Animals, Cell Differentiation, Humans, Oxidation-Reduction, Oxygen Consumption, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Reactive Nitrogen Species, Growth and Development

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