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Recent studies have shown that oxidative stress contributes to the pathogenesis of muscle damage in dystrophic ( mdx ) mice. In this study we have investigated the role of NADPH oxidase as a source of the oxidative stress in these mice. The NADPH oxidase subunits gp91 phox , p67 phox  and rac 1 were increased 2–3 fold in tibilais anterior muscles from  mdx  mice compared to wild type. Importantly, this increase occurred in 19 day old mice, before the onset of muscle necrosis and inflammation, suggesting that NADPH oxidase is an important source of oxidative stress in  mdx  muscle. In muscles from 9 week old  mdx  mice, gp91 phox  and p67 phox  were increased 3–4 fold and NADPH oxidase superoxide production was 2 times greater than wild type. In single fibers from  mdx  muscle NADPH oxidase subunits were all located on or near the sarcolemma, except for p67 phox ,which was expressed in the cytosol. Pharmacological inhibition of NADPH oxidase significantly reduced the intracellular Ca 2+  rise following stretched contractions in  mdx  single fibers, and also attenuated the loss of muscle force. These results suggest that NADPH oxidase is a major source of reactive oxygen species in dystrophic muscle and its enhanced activity has a stimulatory effect on stretch-induced Ca 2+  entry, a key mechanism for muscle damage and functional impairment.

Skeletal Muscle NADPH Oxidase Is Increased and Triggers Stretch-Induced Damage in the mdx Mouse