Inhibition of mitochondrial respiratory complex I by nitric oxide, peroxynitrite and S-nitrosothiols
Open accessAbstract
NO or its derivatives (reactive nitrogen species, RNS) inhibit mitochondrial complex I by several different mechanisms that are not well characterised. There is an inactivation by NO, peroxynitrite and S-nitrosothiols that is reversible by light or reduced thiols, and therefore may be due to S-nitrosation or Fe-nitrosylation of the complex. There is also an irreversible inhibition by peroxynitrite, other oxidants and high levels of NO, which may be due to tyrosine nitration, oxidation of residues or damage of iron sulfur centres. Inactivation of complex I by NO or RNS is seen in cells or tissues expressing iNOS, and may be relevant to inflammatory pathologies, such as septic shock and Parkinson's disease.
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Nitrite-induced S-nitrosation of complex I of the electron transport chain decreases mitochondrial reactive species formation and subsequently confers protection against ischemia-reperfusion injury.
“the nitrite-induced S-nitrosation of complex I of the electron transport chain which decreases mitochondrial reactive species formation and subsequently confers protection against ischemia-reperfusion injury [104] [33, 86, 105, 106].”
From Current perspectives and challenges in understanding the role of nitrite as an integral player in nitric oxide biology and therapy (2011) · cites this paper as [105]
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- Authors
- Brown, G. C., & Borutaite, V.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Brown, Guy C
- ORCID
- Brown, Guy C
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2004-07
- Volume
- 1658
- Issue
- 1-2
- Pages
- 44-49
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W2071051384
- Cited by
- 344
- References
- 52
- Citations by year
- 2026: 8 · 2025: 8 · 2024: 11 · 2023: 11 · 2022: 7 · 2021: 15 · 2020: 17 · 2019: 14 · 2018: 14 · 2017: 20 · 2016: 16 · 2015: 13 · 2014: 21 · 2013: 22 · 2012: 15
- FWCI
- 1.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Lithuanian University of Health Sciences (submittedVersion)
- Funders
- Wellcome Trust
- British Heart Foundation
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- mitochondrial complex I, nitric oxide, peroxynitrite, S-nitrosothiols, reactive nitrogen species, S-nitrosylation, tyrosine nitration, inducible nitric oxide synthase, enzyme inhibition, Parkinson's disease, septic shock, inflammation
- MeSH terms
- Adenosine Triphosphate, Animals, Humans, Iron-Sulfur Proteins, Macrophages, Mitochondria, Nitric Oxide, Nitroso Compounds, Parkinson Disease, Tyrosine, Nitrosation, Nitric Oxide Synthase, Reactive Nitrogen Species, Peroxynitrous Acid, Electron Transport Complex I, Nitric Oxide Synthase Type II
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