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Mitochondrial formation of reactive oxygen species
Open accessAbstract
The reduction of oxygen to water proceeds via one electron at a time. In the mitochondrial respiratory chain, Complex IV (cytochrome oxidase) retains all partially reduced intermediates until full reduction is achieved. Other redox centres in the electron transport chain, however, may leak electrons to oxygen, partially reducing this molecule to superoxide anion (O(2)(−)•). Even though O(2)(−)• is not a strong oxidant, it is a precursor of most other reactive oxygen species, and it also becomes involved in the propagation of oxidative chain reactions. Despite the presence of various antioxidant defences, the mitochondrion appears to be the main intracellular source of these oxidants. This review describes the main mitochondrial sources of reactive species and the antioxidant defences that evolved to prevent oxidative damage in all the mitochondrial compartments. We also discuss various physiological and pathological scenarios resulting from an increased steady state concentration of mitochondrial oxidants.
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“Superoxide anion •O2− is also produced in the mitochondrial matrix at complexes I to IV during the mitochondrial respiration process [10].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [10]
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“Although complexes I and II produce ROS only into the matrix”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [1]
In the citing paper
“complex III can produce ROS on both sides of the mitochondrial inner membrane 1, 3”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [1]
In the citing paper
“Complexes I, II, and III of the electron transport chain contain sites wherein electrons can prematurely reduce oxygen, resulting in the formation of superoxide 1, 2.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [1]
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Metadata
- Authors
- Turrens, J. F.
- Affiliations
- University of South Alabama (US)
- Corresponding author
- Turrens, J. F.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2003-10-15
- Volume
- 552
- Issue
- 2
- Pages
- 335-344
- ISSN
- 0022-3751 (ISSN-L)
- PMC
- PMC2343396
- OpenAlex
- W4247088117
- Cited by
- 5,084
- References
- 112
- Citations by year
- 2026: 134 · 2025: 218 · 2024: 213 · 2023: 277 · 2022: 301 · 2021: 324 · 2020: 324 · 2019: 283 · 2018: 279 · 2017: 302 · 2016: 253 · 2015: 277 · 2014: 289 · 2013: 290 · 2012: 258
- FWCI
- 25.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- reactive oxygen species, mitochondrial respiration, electron transport chain, superoxide, cytochrome c oxidase, electron leakage, antioxidant defense, oxidative damage
- MeSH terms
- Aging, Animals, Antioxidants, Humans, Mitochondria, Nitric Oxide, Oxygen, Superoxides, Xenobiotics, Apoptosis, Reactive Oxygen Species, Oxidative Stress
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