Turnover of muscle and liver proteins in mice with hereditary muscular dystrophy

Results indicate that loss of muscle proteins in myopathic mice is not the result of defective protein synthesis but of increased rate of protein turnover in which the more rapid rate of synthesis is exceeded by an even faster rate of catabolism.

Abstract

Abstract Male mice with hereditary muscular dystrophy and their normal litter mates were injected intravenously with dl -leucine-1-C 14 . The specific radioactivity of skeletal muscle and liver proteins was determined at various intervals following injection. No significant differences were observed between turnovers of liver proteins of dystrophic and normal mice. In marked contrast, turnover of muscle proteins was accelerated in dystrophic mice, with the increase in catabolism apparently exceeding that in synthesis. This increase occurred in myofibrillar as well as sarcoplasmic proteins. These results indicate that loss of muscle proteins in myopathic mice is not the result of defective protein synthesis but of increased rate of protein turnover in which the more rapid rate of synthesis is exceeded by an even faster rate of catabolism.