Artículo
Brain mitochondrial dysfunction in aging
Fecha de publicación:
04/2008
Editorial:
John Wiley & Sons Inc.
Revista:
IUBMB Life
ISSN:
1521-6543
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
Aging of mammalian brain is associated with a continuous decrease of the capacity to produce ATP by oxidative phosphorylation. The impairment of mitochondrial function is mainly due to diminished electron transfer by complexes I and IV, whereas inner membrane H(+) impermeability and F(1)-ATP synthase activity are only slightly affected. Dysfunctional mitochondria in aged rodents show decreased rates of respiration and of electron transfer, decreased membrane potential, increased content of the oxidation products of phospholipids and proteins, and increased size and fragility. In aging mice, the activities of brain mitochondrial enzymes (complexes I and IV and mtNOS) are linearly correlated with neurological performance (tightrope and T-maze tests) and with median life span and negatively correlated with the mitochondrial content of lipid and protein oxidation products. Conditions that increased mice median life span, such as moderate exercise, vitamin E supplementation, caloric restriction, and high spontaneous neurological activity; also improved neurological performance and mitochondrial function in aged brain. The diffusion of mitochondrial NO and H(2)O(2) to the cytosol is decreased in the aged brain and may be a factor for reduced mitochondrial biogenesis.
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Colecciones
Articulos(OCA HOUSSAY)
Articulos de OFICINA DE COORDINACION ADMINISTRATIVA HOUSSAY
Articulos de OFICINA DE COORDINACION ADMINISTRATIVA HOUSSAY
Citación
Boveris, Alberto Antonio; Navarro, Ana; Brain mitochondrial dysfunction in aging; John Wiley & Sons Inc.; IUBMB Life; 60; 5; 4-2008; 308-314
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