A number of studies have reported chronic elevation in intracellular Ca2+ concentration in skeletal muscle fibers or in cultured myotubes from mdx mice (a mouse model for DMD)1. Two of the pathways that might be involved in the Ca2+ overload are store operated calcium channels (SOC) and stretch activated calcium channels (SAC). Earlier results suggest that both channels are controlled, at least partly, by the Ca2+ -independent form of phospholipase A2 (iPLA2)2. In the proposed work, the effect of inhibitors of PLA2, SAC and SOC will be studied using EDL-MDX-2 cell cultures. Selected compounds will be studied in isolated muscle contraction assays to determine their effects on force production, fatigue characteristics and muscular damage