4.7 Article

Long-Term Supplementation With a Cystine-Based Antioxidant Delays Loss of Muscle Mass in Aging

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/gls334

Keywords

Antioxidant; Mice; Muscle cell apoptosis; Oxidative stress; Sarcopenia

Funding

  1. American Federation of Aging Research
  2. National Institutes of Health [U54MD007598, U54RR026138, P20MD00182, 3P30AG021684]

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Oxidative stress increases with age and is postulated to be a major causal factor for sarcopenia in aging. Here, we examined whether the administration of a cystine-based antioxidant (F1) can alleviate/delay age-specific changes in skeletal muscles. C57BL6 male mice aged 17 months (middle aged) were fed with normal diet with or without supplementation of F1 (3 mg/kg food) for 6 months. Compared with young (5 months old) mice old mice exhibited increased markers of oxidative stress, inflammation, and muscle cell apoptosis and decreased muscle weight. These age-related changes were further associated with inactivation of adenosine-5'-monophosphate-activated protein kinase (AMPK), increased lipogenesis, activation of c-Jun NH2-terminal kinase, and decreased expression of Delta 1, phospho-Akt, and proliferating cell nuclear antigen in aged skeletal muscle. Such alterations were significantly prevented by F1. These results demonstrate the beneficial effects of F1 to attenuate loss of muscle mass associated with aging.

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