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1 Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Cadiz, 11003-Cadiz, Cadiz, Spain
2 Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, C1113AAD Buenos Aires, Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: ana.navarro{at}uca.es.
The mitochondrial mass of rat brain and liver remained unchanged upon aging in young adults, old adults and senescent animals (28, 60 and 92 wk of age); the values were 15-17 and 29-31 mg protein/g, for brain and liver, respectively. The whole aging process was associated to an increased content of the oxidation products, TBARS and protein carbonyls, by 61-69 % in brain and 36-45 % in liver, respectively. The activities of critical enzymes for mitochondrial function: mitochondrial nitric oxide synthase, Mn-superoxide dismutase, complex I and complex IV, decreased progressively during aging with activity losses of 73, 37, 29 and 28 %, respectively, in the brain, and 47, 46, 30 and 24 % in the liver of senescent rats, as compared with young adults. Brain mitochondria isolated from aged rats showed increased mitochondrial fragility, as assayed by mitochondrial marker enzyme activities in the post-mitochondrial supernatant, and increased volume and water permeability, as assayed by light scattering. Liver mitochondria isolated from young and old rats did not show differences in fragility and water permeability. A subpopulation of brain mitochondria with increased size and fragility was differentiated in aging rats, whereas liver showed an homogeneous mitochondrial population.
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