Effect of lifestyle on age-related mitochondrial protein oxidation in mice cardiac muscle

• DOI: 10.1007/s00421-011-2100-3
• Publication Date: 2011-08-10T06:15:45Z
• Authors: Ana Isabel Padrão; Rita Ferreira; Rui Vitorino; Renato M. P. Alves; Pedro Figueiredo; José Alberto Duarte; Francisco Amado
• Keywords: Male; 2. Zero hunger; Aging; 0303 health sciences; Superoxide Dismutase; Myocardium; Physical Exertion; Age Factors; Lipid Metabolism; Mitochondria, Heart; Oxidative Phosphorylation; Running; Mice, Inbred C57BL; Mitochondrial Proteins; Protein Carbonylation; Mice; 03 medical and health sciences; Electron Transport Chain Complex Proteins; Animals; Sedentary Behavior; Oxidation-Reduction

This study investigated the influence of lifestyle on aging-related changes in cardiac proteins' oxidative modifications profile. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young Y, old sedentary S, and old active A). The S and A mice were individually placed into standard cages and in cages with running wheels, respectively, for 23 months. Upon killing, heart mitochondrial fractions were obtained for the evaluation of general proteins oxidative modifications profile, the identification of preferential protein targets, and oxidative phosphorylation (OXPHOS) activity. We observed age-related cardiac muscle impairment, evidenced by decreased OXPHOS activity, paralleled by an increased protein susceptibility to carbonylation and nitration. Among the main targets to these posttranslational modifications we found mitochondrial proteins, mainly from OXPHOS complexes, MnSOD and enzymes from lipid metabolism. Lifelong sedentary behavior exacerbated the nitrative damage of mitochondrial proteins, paralleled by a statistically significant decrease of respiratory chain complexes II and III activities. In overall, our results highlight the determinant role of aging in cardiac muscle impairment, which is worsened by a sedentary lifestyle.