An investigation of oxidative stress in skeletal muscle

Abstract

Reactive oxygen species (ROS) are produced as a by-product of oxidative phosphorylation in mitochondria and via various cellular enzyme systems. ROS production is buffered by cellular antioxidant defences, which include superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), vitamin C & E. hi certain circumstances, such as exercise and aging, the production of ROS in skeletal muscle increases significantly. Without adequate antioxidant defences, an oxidative stress can occur that induces damage and/or modification to cellular organelles and can result in altered cell function. In skeletal muscle, ROS have been shown to oxidize critical proteins involved in excitation-contraction coupling and the cross-bridge power stroke, which directly affects skeletal muscle force output. Deterioration in the structure and function of skeletal muscle with age, as measured by muscle atrophy, in conjunction with a diminished ability to maintain force and a loss in overall muscle strength, has been partly attributed to an increase in basal levels of ROS and reduced antioxidant defences.