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Cited by 650Mitochondrial Function and PathologyAutophagy in Disease and TherapyGenetics, Aging, and Longevity in Model Organisms

Role of mitochondria in oxidative stress and ageing

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Lenaz, Giorgio·1998·Biochimica et Biophysica Acta (BBA) - Bioenergetics
DOI 10.1016/s0005-2728(98)00120-0
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Abstract

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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  • The mitochondrial respiratory chain produces partially reduced dioxygen species such as hydrogen peroxide and superoxide at considerable rates (ca 1-4% of O2 reduced) even under normal conditions and during ischaemia.

    “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”

    From Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases (2009) · cites this paper as [28]

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Research works printed but not linked: 23

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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)
DOI
10.1016/s0005-2728(98)00120-0
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
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
  • Health Sciences › Medicine › Epidemiology › 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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