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Updated: Oct 17, 2026

Imaging of mtHyPer7, a Ratiometric Biosensor for Mitochondrial Peroxide, in Living Yeast Cells
Published on: June 2, 2023
Mitochondria, oxidative stress and aging
J Sastre1, F V Pallardó, J García de la Asunción
1Facultad de Medicina, Departamento de Fisiología, Universitat de Valencia, Spain.
Abstract:
In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDNA), are major targets of free radical attack. At present, it is well established that mitochondrial deficits accumulate upon aging due to oxidative damage. Thus, oxidative lesions to mtDNA accumulate with age in human and rodent tissues. Furthermore, levels of oxidative damage to mtDNA are several times higher than those of nuclear DNA. Mitochondrial size increases whereas mitochondrial membrane potential decreases with age in brain and liver. Recently, we have shown that treatment with certain antioxidants, such as sulphur-containing antioxidants, vitamins C and E or the Ginkgo biloba extract EGb 761, protects against the age-associated oxidative damage to mtDNA and oxidation of mitochondrial glutathione. Moreover, the extract EGb 761 also prevents changes in mitochondrial morphology and function associated with aging of the brain and liver. Thus, mitochondrial aging may be prevented by antioxidants. Furthermore, late onset administration of certain antioxidants is also able to prevent the impairment in physiological performance, particularly motor co-ordination, that occurs upon aging.
Insights
Antioxidants can prevent cellular aging by protecting mitochondrial DNA from oxidative damage. Late-onset antioxidant treatment also improves age-related decline in physiological functions like motor coordination.
Area of Science:
- Gerontology
- Mitochondrial Biology
- Oxidative Stress Research
Background:
- Mitochondria and their DNA (mtDNA) are susceptible to oxidative damage, accumulating with age.
- Age-related mitochondrial dysfunction is linked to cellular aging and declines in physiological performance.
- Oxidative damage to mtDNA is significantly higher than to nuclear DNA.
Purpose of the Study:
- To investigate the role of antioxidants in preventing age-associated oxidative damage to mitochondria.
- To determine if antioxidant treatment can reverse or prevent age-related changes in mitochondrial morphology and function.
- To assess the efficacy of late-onset antioxidant administration in mitigating age-related physiological impairments.
Main Methods:
- Treatment with various antioxidants including sulfur-containing compounds, vitamins C and E, and Ginkgo biloba extract (EGb 761).
- Assessment of oxidative damage to mitochondrial DNA (mtDNA) and mitochondrial glutathione.
- Evaluation of changes in mitochondrial size and membrane potential in brain and liver tissues.
- Analysis of physiological performance, specifically motor coordination, following antioxidant treatment.
Main Results:
- Antioxidants, particularly EGb 761, protected against age-associated oxidative damage to mtDNA and mitochondrial glutathione.
- EGb 761 prevented age-related alterations in mitochondrial morphology and function in brain and liver.
- Late-onset antioxidant administration reversed age-related declines in physiological performance, including motor coordination.
Conclusions:
- Antioxidant interventions can effectively prevent mitochondrial aging and its associated cellular damage.
- Targeting mitochondrial oxidative stress with antioxidants offers a promising strategy for combating age-related decline.
- Antioxidants may serve as therapeutic agents to improve physiological function in aging populations.
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