title: Melatonin administration prevents cardiac and diaphragmatic mitochondrial oxidative damage in senescence-accelerated mice.
abstract: Cardiac and diaphragmatic mitochondria from male SAMP8 (senescent) and SAMR1 (resistant) mice of 5 or 10 months of age were studied. Levels of lipid peroxidation (LPO), glutathione (GSH), GSH disulfide (GSSG), and GSH peroxidase and GSH reductase (GRd) activities were measured. In addition, the effect of chronic treatment with the antioxidant melatonin from 1 to 10 months of age was evaluated. Cardiac and diaphragmatic mitochondria show an age-dependent increase in LPO levels and a reduction in GSH:GSSG ratios. Chronic treatment with melatonin counteracted the age-dependent LPO increase and GSH:GSSG ratio reduction in these mitochondria. Melatonin also increased GRd activity, an effect that may account for the maintenance of the mitochondrial GSH pool. Total mitochondrial content of GSH increased after melatonin treatment. In general, the effects of age and melatonin treatment were similar in senescence-resistant mice (SAMR1) and SAMP8 cardiac and diaphragmatic mitochondria, suggesting that these mice strains display similar mitochondrial oxidative damage at the age of 10 months. The results also support the efficacy of long-term melatonin treatment in preventing the age-dependent mitochondrial oxidative stress.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Instituto de Biotecnología, Universidad de Granada, Avenida de Madrid 11, E-18012 Granada, Spain.
authors.forename: M I
authors.initials: MI
authors.lastname: Rodriguez
authors.forename: G
authors.initials: G
authors.lastname: Escames
authors.forename: L C
authors.initials: LC
authors.lastname: López
authors.forename: J A
authors.initials: JA
authors.lastname: García
authors.forename: F
authors.initials: F
authors.lastname: Ortiz
authors.forename: A
authors.initials: A
authors.lastname: López
authors.forename: D
authors.initials: D
authors.lastname: Acuña-Castroviejo
mesh_terms: D019588:Aging, Premature / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D003964:Diaphragm; D005978:Glutathione / Q000032:analysis; D019803:Glutathione Disulfide / Q000032:analysis; D005979:Glutathione Peroxidase / Q000032:analysis; D005980:Glutathione Reductase / Q000032:analysis; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008550:Melatonin / Q000494:pharmacology*; D051379:Mice; D008817:Mice, Mutant Strains; D008928:Mitochondria / Q000737:chemistry / Q000187:drug effects* / Q000378:metabolism; D008929:Mitochondria, Heart / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects
chemical_list: D000975:Antioxidants; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005978:Glutathione; D008550:Melatonin; D019803:Glutathione Disulfide