Protein synthesis and antioxidant capacity in ageing mice: effects of life-long cold exposure

Substantial evidence supports a key role for reactive oxygen species (ROS) in causing cumulative damage to cellular macromolecules, thereby contributing to senescence. Antioxidants can scavenge ROS while protein turnover removes and replaces oxidized proteins. How these defence systems vary with age and with metabolic demand is not well known. In the present study 2H5-phenylalanine was injected into young (3 months) and old (27 months) mice chronically exposed to cold to explore effects of cold exposure on age-related changes in liver and muscle protein synthesis. In addition, effects of cold exposure (10∞C) on antioxidant enzyme activities were investigated in two metabolically active tissues in mice at various ages (3-27 months). Cold exposure did not affect fractional synthesis rates (FSR) in liver or muscle. FSR rates did decrease with age in both tissues, and in liver this occurred more rapidly in cold-exposed animals than in controls. Antioxidant enzyme activity (SOD and GPx) was also affected by age. SOD activity peaked in 11 month old mice followed by a decline, while GPx activity slowly declined with age. SOD activity in heart was unaffected by cold. In liver, SOD activity was decreased in cold-exposed animals, but GPx activity was not. No relationship between energy expenditure and enzyme activity was found. Cold exposure increased metabolic rate by approximately 40% with no concurrent increase in antioxidant enzyme activity. Cold-exposed animals did not up-regulate either protein synthesis or antioxidant enzyme activities to provide protection against extra production of ROS. Chapter9