Chronic melatonin treatment prevents age-dependent cardiac mitochondrial dysfunction in senescence-accelerated mice

María I. Rodríguez, Miguel Carretero, Germaine Escames, Luis C. López, María D. Maldonado, Dun Xian Tan, Russel J. Reiter, Darío Acuña-Castroviejo

Research output: Contribution to journalArticlepeer-review

72 Scopus citations

Abstract

Heart mitochondria from female senescence-accelerated (SAMP8) and senescence-resistant (SAMR1) mice of 5 or 10 months of age, were studied. Mitochondrial oxidative stress was determined by measuring the levels of lipid peroxidation, glutathione and glutathione disulfide and glutathione peroxidase and reductase activities. Mitochondrial function was assessed by measuring the activity of the respiratory chain complexes and ATP content. The results show that the age-dependent mitochondrial oxidative damage in the heart of SAMP8 mice was accompanied by a reduction in the electron transport chain complex activities and in ATP levels. Chronic melatonin administration between 1 and 10 months of age normalized the redox and the bioenergetic status of the mitochondria and increased ATP levels. The results support the presence of significant mitochondrial oxidative stress in SAM mice at 10 months of age, and they suggest a beneficial effect of chronic pharmacological intervention with melatonin, which reduces the deteriorative and functional oxidative changes in cardiac mitochondria with age.

Original languageEnglish (US)
Pages (from-to)15-24
Number of pages10
JournalFree Radical Research
Volume41
Issue number1
DOIs
StatePublished - Jan 1 2007

Keywords

  • Aging
  • Heart
  • Melatonin treatment
  • Mitochondria
  • Oxidative damage

ASJC Scopus subject areas

  • Biochemistry

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