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Oxidative stress, antioxidant defences and aging
G Lenaz1, M Cavazzoni, M L Genova
1Dipartimento di Biochimica G. Moruzzi, Università di Bologna, Italy. lenaz@biocfarm.unibo.it
Biofactors (Oxford, England)
|January 23, 1999
Summary
Oxidative stress and mitochondrial dysfunction are key in aging and apoptosis. Coenzyme Q10 demonstrated antioxidant effects, while aging-related mitochondrial decline may not solely stem from DNA lesions.
Area of Science:
- Biochemistry
- Cell Biology
- Gerontology
Background:
- Apoptosis and aging share common mechanisms, including oxidative stress and mitochondrial dysfunction.
- Mitochondrial involvement in cell death pathways is critical in both aging and apoptosis.
- Oxidative stress plays a significant role in cellular damage and aging processes.
Purpose of the Study:
- To investigate the shared mechanisms between apoptosis and aging, focusing on oxidative stress and mitochondria.
- To evaluate the protective effects of Coenzyme Q10 against drug-induced mitochondrial damage.
- To explore age-related changes in mitochondrial function and their potential causes.
Main Methods:
- Induction of apoptosis in neuroblastoma cells using a radical initiator.
- Treatment of rat hepatocytes with adriamycin and exogenous Coenzyme Q10.
- Analysis of mitochondrial Complex I activity and rotenone sensitivity in aged rat brain cortex mitochondria.
- Detection of mitochondrial DNA deletions in aged rat and human samples.
- Assessment of platelet aggregation and lactate production in aged individuals.
Main Results:
- Radical initiator treatment induced apoptosis, characterized by increased hydrogen peroxide, cytochrome c release, and mitochondrial potential collapse.
- Coenzyme Q10 counteracted adriamycin-induced hydrogen peroxide increase and mitochondrial potential decrease in rat hepatocytes.
- Aged rat brain mitochondria showed decreased Complex I activity and increased rotenone sensitivity, with a 5 kb mitochondrial DNA deletion.
- Similar mitochondrial dysfunction was observed in platelets from old individuals, but without the 5 kb deletion.
- Energy decline in aged platelets was confirmed by altered inhibitor sensitivities.
Conclusions:
- Exogenous Coenzyme Q10 exhibits antioxidant effects, protecting against mitochondrial dysfunction.
- Mitochondrial dysfunction in aging is complex and may not be solely attributed to mitochondrial DNA lesions.
- Shared pathways involving oxidative stress and mitochondria link apoptosis and aging.