期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 40, 期 11, 页码 1993-2004出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2006.01.036
关键词
superoxide; muscle atrophy; aging; oxidative stress; CuZnSOD; free radicals
资金
- NIA NIH HHS [5T3-AG021890-02, P01 AG20591] Funding Source: Medline
- NIGMS NIH HHS [GM42056] Funding Source: Medline
We describe a novel phenotype in mice lacking the major antioxidant enzyme, CuZn-superoxide dismutase (Sod1(-/-) mice), namely a dramatic acceleration of age-related loss of skeletal muscle mass. Sod1(-/-) mice are 17 to 20% smaller and have a significantly lower muscle mass than wildtype mice as early as 3 to 4 months of age. Muscle mass in the Sod1(-/-) mice is further reduced with age and by 20 months, the hind-limb muscle mass in Sod1(-/-) mice is nearly 50% lower than in age-matched wild-type mice. Skeletal muscle tissue from young Sod1(-/-) mice has elevated oxidative damage to proteins, lipids, and DNA compared to muscle from young wild-type mice. The reduction in muscle mass and elevated oxidative damage are accompanied by a 40% decrease in voluntary wheel running by 6 months of age and decreased performance on the Rota-rod test at 13 months of age, but are not associated with a decline in overall spontaneous activity. In some of the old Sod1(-/-) mice, the loss in muscle mass is also associated with the presence of tremors and gait disturbances. Thus, the absence of CuZnSOD imposes elevated oxidative stress, loss of muscle mass, and physiological consequences that resemble an acceleration of normal age-related sarcopenia. (c) 2006 Elsevier Inc. All rights reserved.
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