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Oxidative stress in skeletal muscle causes severe disturbance of exercise activity without muscle atrophy.
Free Radic Biol Med ; 48(9): 1252-62, 2010 May 01.
Article en En | MEDLINE | ID: mdl-20156551
The increase in reactive oxygen species (ROS) levels that occurs during intense exercise has been proposed to be one of the major causes of muscle fatigue. In addition, the accumulation of cellular damage due to ROS is widely regarded to be one of the factors triggering age-related pathological conditions in skeletal muscle. To investigate the pathological significance of oxidative stress in skeletal muscle, we generated skeletal muscle-specific manganese superoxide dismutase-deficient (muscle-Sod2(-/-)) mice. The mutant mice showed severe disturbances in exercise activity, but no atrophic changes in their skeletal muscles. In histological and histochemical analyses, the mutant mice showed centralized nuclei in their muscle fibers and selective loss of enzymatic activity in mitochondrial respiratory chain complexes. In addition, the mutant mice displayed increased oxidative damage and reduced ATP content in their muscle tissue. Furthermore, a single administration of the antioxidant EUK-8 significantly improved exercise activity and increased the cellular ATP level in skeletal muscle. These results imply that the superoxide anions generated in mitochondria play a pivotal role in the progression of exercise intolerance.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Condicionamiento Físico Animal / Atrofia Muscular / Estrés Oxidativo / Músculo Esquelético / Mitocondrias Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: Free Radic Biol Med Asunto de la revista: BIOQUIMICA / MEDICINA Año: 2010 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Condicionamiento Físico Animal / Atrofia Muscular / Estrés Oxidativo / Músculo Esquelético / Mitocondrias Tipo de estudio: Etiology_studies Límite: Animals Idioma: En Revista: Free Radic Biol Med Asunto de la revista: BIOQUIMICA / MEDICINA Año: 2010 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos