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Cited by 1,133Redox biology and oxidative stressAntioxidant Activity and Oxidative StressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Reactive oxygen species: from health to disease

Open access
Brieger, Katharine, Schiavone, Stefania, Miller Jr., Francis J., Krause, Karl-Heinz·2012·Swiss Medical Weekly
DOI 10.4414/smw.2012.13659
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Abstract

Upon reaction with electrons, oxygen is transformed into reactive oxygen species (ROS). It has long been known that ROS can destroy bacteria and destroy human cells, but research in recent decades has highlighted new roles for ROS in health and disease. Indeed, while prolonged exposure to high ROS concentrations may lead to non-specific damage to proteins, lipids, and nucleic acids, low to intermediate ROS concentrations exert their effects rather through regulation of cell signalling cascades. Biological specificity is achieved through the amount, duration, and localisation of ROS production. ROS have crucial roles in normal physiological processes, such as through redox regulation of protein phosphorylation, ion channels, and transcription factors. ROS are also required for biosynthetic processes, including thyroid hormone production and crosslinking of extracellular matrix. There are multiple sources of ROS, including NADPH oxidase enzymes; similarly, there are a large number of ROS-degrading systems. ROS-related disease can be either due to a lack of ROS (e.g., chronic granulomatous disease, certain autoimmune disorders) or a surplus of ROS (e.g., cardiovascular and neurodegenerative diseases). For diseases caused by a surplus of ROS, antioxidant supplementation has proven largely ineffective in clinical studies, most probably because their action is too late, too little, and too non-specific. Specific inhibition of ROS-producing enzymes is an approach more promising of clinical efficacy.

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Cited by

Sorted by citations

Authors
Brieger, K., Schiavone, S., Miller Jr., F. J., & Krause, K.-H.
Affiliations
University of Geneva (CH)
ORCID
Venue
Swiss Medical Weekly
Publisher
SMW Supporting Association
Published
2012-08-12
Volume
142
Issue
3334
Pages
w13659
ISSN
  • 0036-7672 (ISSN-L)
  • 1424-3997
DOI
10.4414/smw.2012.13659
OpenAlex
W1983019829
Cited by
1,133
References
8
Citations by year
2026: 62 · 2025: 109 · 2024: 112 · 2023: 151 · 2022: 140 · 2021: 111 · 2020: 82 · 2019: 72 · 2018: 50 · 2017: 53 · 2016: 52 · 2015: 48 · 2014: 56 · 2013: 31
FWCI
3.94
Type
journal article
Language
en
Open access
Licence
Locations
  • Swiss Medical Weekly (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Keywords
reactive oxygen species, redox signaling, NADPH oxidase, antioxidant supplementation, chronic granulomatous disease, autoimmune disease, cardiovascular disease, neurodegenerative diseases, protein phosphorylation, ion channels, transcription factors, thyroid hormone synthesis, extracellular matrix cross-linking
MeSH terms
Aging, Antioxidants, Mental Disorders, Cardiovascular Diseases, Cognition, Humans, Immunity, Neoplasms, Nervous System Diseases, Thyroid Gland, Vision Disorders, Reactive Oxygen Species, NADPH Oxidases, Hearing Loss

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