Mitochondria, oxidative stress and aging

Citation
J. Sastre et al., Mitochondria, oxidative stress and aging, FREE RAD RE, 32(3), 2000, pp. 189-198
Citations number
108
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL RESEARCH
ISSN journal
10715762 → ACNP
Volume
32
Issue
3
Year of publication
2000
Pages
189 - 198
Database
ISI
SICI code
1071-5762(2000)32:3<189:MOSAA>2.0.ZU;2-I
Abstract
In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDN A), are major targets of free radical attack. At present, it is well establ ished that mitochondrial deficits accumulate upon aging due to oxidative da mage. Thus, oxidative lesions to mtDNA accumulate with age in human and rod ent tissues. Furthermore, levels of oxidative damage to mtDNA are several t imes 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 s ulphur-containing antioxidants, vitamins C and E or the Ginkgo biloba extra ct EGb 761, protects against the age-associated oxidative damage to mtDNA a nd oxidation of mitochondrial glutathione. Moreover, the extract EGb 761 al so prevents changes in mitochondrial morphology and function associated wit h aging of the brain and liver. Thus, mitochondrial aging may be prevented by antioxidants. Furthermore, late onset administration of certain antioxid ants is also able to prevent the impairment in physiological performance, p articularly motor co-ordination, that occurs upon aging.