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Issue 959 coverINCREASING HEALTHY LIFE SPAN: CONVENTIONAL MEASURES AND SLOWING THE INNATE AGING PROCESS Copyright © 2002 by the New York Academy of Sciences
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Annals of the New York Academy of Sciences 959:448-451 (2002)
© 2002 New York Academy of Sciences

Mitochondrial Damage in Aging and Apoptosis

JUAN SASTRE, CONSUELO BORRÁS, DAVID GARCÍA-SALA, ANA LLORET, FEDERICO V. PALLARDÓ AND JOSÉ VIÑA

Departamento de Fisiología, Facultad de Medicina, Universidad de Valencia, Avda. Blasco Ibañez 17, 46010 Valencia, Spain

Address for correspondence: Dr. José Viña, Departamento de Fisiología, Facultad de Medicina, Universitat de Valencia, Avda. Blasco Ibañez 17, 46010 Valencia, Spain. Voice: +34-96-386-46-46; fax: +34-96-386-46-42.
jose.vina{at}uv.es
Ann. N.Y. Acad. Sci. 959: 448-451 (2002).

Mitochondria are essential to cellular aging, and free radical production by mitochondria is increased with aging. The rate of oxidant production by mitochondria correlates inversely with maximal life span of species. In many species, females live longer than males. We report that mitochondrial oxidant production by females is significantly lower than that of males. However, mitochondria from ovariectomized females have a similar oxidant production as those of males. Thus, gender difference in life span can be explained, at least in part, by different oxidant generation by mitochondria. Administration of antioxidants, such as vitamins C and E, or a Ginkgo biloba extract, protects against age-associated oxidative damage to mitochondrial DNA, oxidation of glutathione, and other signs of oxidative damage to mitochondria.

Key Words: mitochondria • aging • free radicals • antioxidants • vitamins




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