Mitochondria and reactive oxygen species

Kowaltowski, Alicia J.; de Souza-Pinto, Nadja C.; Castilho, Roger F.; Vercesi, Anibal E.

doi:10.1016/j.freeradbiomed.2009.05.004

Cited by 1,162Mitochondrial Function and PathologyRedox biology and oxidative stressAutophagy in Disease and Therapy

Mitochondria and reactive oxygen species

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Kowaltowski, Alicia J., de Souza-Pinto, Nadja C., Castilho, Roger F., Vercesi, Anibal E.·2009·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2009.05.004

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Abstract

Mitochondria are a quantitatively relevant source of reactive oxygen species (ROS) in the majority of cell types. Here we review the sources and metabolism of ROS in this organelle, including the conditions that regulate the production of these species, such as mild uncoupling, oxygen tension, respiratory inhibition, Ca2+ and K+ transport, and mitochondrial content and morphology. We discuss substrate-, tissue-, and organism-specific characteristics of mitochondrial oxidant generation. Several aspects of the physiological and pathological roles of mitochondrial ROS production are also addressed.

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In the presence of these inhibitors, the highly reduced state of components of the electron transport system causes a rise in the production of superoxide at these sites, which would be a challenge to cell survival.
“In the presence of these inhibitors, the highly reduced state of components of the electron transport system causes a rise in the production of superoxide at these sites [47,48], which would be a challenge to cell survival.”
From Proliferating Astrocytes in Primary Culture Do Not Depend upon Mitochondrial Respiratory Complex I Activity or Oxidative Phosphorylation (2023) · cites this paper as [48]
Mitochondrial deficiencies that decrease matrix NADH or mitochondrial membrane potential will theoretically decrease mitochondrial NADPH regeneration, contributing to oxidative stress.
“Thus, mitochondrial deficiencies that decrease matrix NADH or mitochondrial membrane potential will theoretically decrease mitochondrial NADPH regeneration, contributing to oxidative stress (226).”
From Redox regulation of mitochondrial function (2012) · cites this paper as [226]

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Mitochondrial metabolism of reactive oxygen species
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Authors: Kowaltowski, A. J., de Souza-Pinto, N. C., Castilho, R. F., & Vercesi, A. E.
Affiliations: Universidade de São Paulo (BR)
Universidade Estadual de Campinas (UNICAMP) (BR)
ORCID: Kowaltowski, Alicia J.
Castilho, Roger F.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2009-08
Volume: 47
Issue: 4
Pages: 333-343
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2009.05.004
OpenAlex: W2016693012
Cited by: 1,162
References: 235
Citations by year: 2026: 39 · 2025: 48 · 2024: 52 · 2023: 72 · 2022: 51 · 2021: 77 · 2020: 76 · 2019: 52 · 2018: 70 · 2017: 68 · 2016: 70 · 2015: 76 · 2014: 91 · 2013: 98 · 2012: 82
FWCI: 5.45
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 280 d)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: Fundação de Amparo à Pesquisa do Estado de São Paulo
Conselho Nacional de Desenvolvimento Científico e Tecnológico
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 › Epidemiology › Autophagy in Disease and Therapy
Keywords: mitochondria, reactive oxygen species, mitochondrial ROS production, mitochondrial uncoupling, oxygen partial pressure, respiratory inhibition, calcium transport, potassium transport, mitochondrial morphology, mitochondrial content
MeSH terms: Aging, Animals, Calcium, Electron Transport, Humans, Mitochondria, Potassium, Respiration, Signal Transduction, Reactive Oxygen Species, Proton Pumps, Oxidative Stress, Feedback, Physiological

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