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Role of mitochondria in oxidative stress and ageing
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Mitochondria are deeply involved in the production of reactive oxygen species through one-electron carriers in the respiratory chain; mitochondrial structures are also very susceptible to oxidative stress as evidenced by massive information on lipid peroxidation, protein oxidation, and mitochondrial DNA (mtDNA) mutations. Oxidative stress can induce apoptotic death, and mitochondria have a central role in this and other types of apoptosis, since cytochrome c release in the cytoplasm and opening of the permeability transition pore are important events in the apoptotic cascade. The discovery that mtDNA mutations are at the basis of a number of human pathologies has profound implications: maternal inheritance of mtDNA is the basis of hereditary mitochondrial cytopathies; accumulation of somatic mutations of mtDNA with age has represented the basis of the mitochondrial theory of ageing, by which a vicious circle is established of mtDNA damage, altered oxidative phosphorylation and overproduction of reactive oxygen species. Experimental evidence of respiratory chain defects and of accumulation of multiple mtDNA deletions with ageing is in accordance with the mitochondrial theory, although some other experimental findings are not directly ascribable to its postulates.
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“Even under 'normal' conditions, as well as during ischaemia when tissue oxygenation levels are low, the redox poise of the mitochondrial respiratory chain is such that the normally complete four-electron reduction of dioxygen to water is also accompanied by the production, at considerable rates (ca 1–4% of O2 reduced), of partially reduced forms of dioxygen such as hydrogen peroxide and superoxide”
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Metadata
- Authors
- Lenaz, G.
- Affiliations
- University of Bologna (IT)
- Corresponding author
- Lenaz, Giorgio
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 1998-08
- Volume
- 1366
- Issue
- 1-2
- Pages
- 53-67
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W2016486229
- Cited by
- 650
- References
- 206
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 9 · 2023: 10 · 2022: 22 · 2021: 23 · 2020: 15 · 2019: 16 · 2018: 15 · 2017: 9 · 2016: 25 · 2015: 12 · 2014: 24 · 2013: 25 · 2012: 21
- FWCI
- 10.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondria, oxidative stress, aging, reactive oxygen species, electron transport chain, lipid peroxidation, protein oxidation, mitochondrial DNA mutations, mitochondrial DNA deletions, apoptosis, cytochrome c release, mitochondrial permeability transition pore, oxidative phosphorylation, maternal inheritance, somatic mtDNA mutations
- MeSH terms
- Aging, Animals, DNA Damage, DNA, Mitochondrial, Energy Metabolism, Free Radicals, Humans, Mitochondria, Mutation, Cell Death, Reactive Oxygen Species, Oxidative Stress, Neurodegenerative Diseases
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