The mitochondrial energy transduction system and the aging process
Abstract
Aged mammalian tissues show a decreased capacity to produce ATP by oxidative phosphorylation due to dysfunctional mitochondria. The mitochondrial content of rat brain and liver is not reduced in aging and the impairment of mitochondrial function is due to decreased rates of electron transfer by the selectively diminished activities of complexes I and IV. Inner membrane H(+) impermeability and F(1)-ATP synthase activity are only slightly affected by aging. Dysfunctional mitochondria in aged rodents are characterized, besides decreased electron transfer and O(2) uptake, by an increased content of oxidation products of phospholipids, proteins and DNA, a decreased membrane potential, and increased size and fragility. Free radical-mediated oxidations are determining factors of mitochondrial dysfunction and turnover, cell apoptosis, tissue function, and lifespan. Inner membrane enzyme activities, such as those of complexes I and IV and mitochondrial nitric oxide synthase, decrease upon aging and afford aging markers. The activities of these three enzymes in mice brain are linearly correlated with neurological performance, as determined by the tightrope and the T-maze tests. The same enzymatic activities correlated positively with mice survival and negatively with the mitochondrial content of lipid and protein oxidation products. Conditions that increase survival, as vitamin E dietary supplementation, caloric restriction, high spontaneous neurological activity, and moderate physical exercise, ameliorate mitochondrial dysfunction in aged brain and liver. The pleiotropic signaling of mitochondrial H(2)O(2) and nitric oxide diffusion to the cytosol seems modified in aged animals and to contribute to the decreased mitochondrial biogenesis in old animals.
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Mitochondrial function declines throughout much of adulthood, and adaptive changes at least initially mitigate this decline.
“Existing data suggest mitochondrial function declines throughout much of adulthood and that adaptive changes, at least initially, mitigate this decline [47, 80-82].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [81]
Mitochondrial changes occur with advancing age.
“Numerous studies certainly find mitochondrial changes occur with advancing age [106, 107].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [107]
Electron transport chain function declines, while free radical production increases with age.
“Electron transport chain function declines, while free radical production increases.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [107]
Age-related mitochondrial changes include a decline in complex I and complex IV activity, with preserved complex II activity.
“Within the brain, age-related mitochondrial changes include a decline in complex I (NADH:ubiquinone oxidoreductase) and complex IV (cytochrome oxidase; COX) activity, with preserved complex II (succinate dehydrogenase) activity [107].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [107]
With advancing age, mitochondrial function and dynamics change.
“With advancing age, mitochondrial function and dynamics change.”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [107]
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- Authors
- Navarro, A., & Boveris, A.
- Affiliations
- Universidad de Cádiz (ES)
- ORCID
- Navarro, Ana
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2007-02
- Volume
- 292
- Issue
- 2
- Pages
- C670-C686
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- OpenAlex
- W2113333476
- Cited by
- 646
- References
- 166
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 22 · 2023: 21 · 2022: 19 · 2021: 28 · 2020: 24 · 2019: 27 · 2018: 27 · 2017: 35 · 2016: 28 · 2015: 46 · 2014: 36 · 2013: 56 · 2012: 57
- FWCI
- 12.89
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Cell Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, aging, oxidative phosphorylation, complex I, cytochrome c oxidase, F1-ATP synthase, mitochondrial membrane potential, lipid peroxidation, protein oxidation, DNA oxidation, mitochondrial nitric oxide synthase, free radical oxidation, apoptosis, lifespan, brain aging, liver aging, vitamin E supplementation, caloric restriction, physical activity, mitochondrial biogenesis, hydrogen peroxide, nitric oxide, mitochondrial energy transduction
- MeSH terms
- Aging, Animals, Electron Transport, Energy Metabolism, Proton-Translocating ATPases, Humans, Hydrogen Peroxide, Mitochondria, Oxidative Phosphorylation, Oxygen Consumption, Cell Death, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Mitochondrial Membranes, Mice, Rats
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