期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 48, 期 9, 页码 1252-1262出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2010.02.011
关键词
Reactive oxygen species; Superoxide anions; Manganese superoxide dismutase; Oxidative stress; Mitochondria; Free radicals
资金
- Program for the Promotion of Basic Research Activities for Innovative Biosciences
- Ministry of Education, Science, Culture, Sports, and Technology [17390085, 20390085, 20500641, 17790201]
- Grants-in-Aid for Scientific Research [17390085, 20390085, 17790201, 20500641] Funding Source: KAKEN
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. (C) 2010 Elsevier Inc. All rights reserved.
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