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Contents of reduced glutathione were also augmented in response to such UV-C radiation exposure [12]

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Introduction It has been proposed that oxidative stress plays a role in the pathophysiology of Duchenne Muscular Dystrophy (DMD), despite this there is currently no effective antioxidant treatment for DMD ( Several studies have used the mdx dystrophin deficient mouse, the most used animal model of the destructive human dystrophin deficient muscular dystrophy DMD, to study the chronic effects of oral administration of NAC in drinking water or by intraperitoneal injection on skeletal muscle pathology ( There have been reports of a reduction in body weight gain in mice chronically dosed with NAC in their drinking water ( Previous studies from our laboratory and others have demonstrated a characteristic feature of the dystrophic pathology in mdx mice and DMD boys are the presence of abnormally regenerated branched limb skeletal muscle fibers which increase in number and complexity with age ( Since the first reports of the mdx mouse it has been noted that the fast-twitch muscles are more susceptible to eccentric (lengthening) contraction (EC) damage ( To test the efficacy of NAC as a possible treatment for DMD we gave it orally for 6 weeks to growing mdx and control mice and measured its effect on body weight gain, EDL muscle weight, fiber branching morphology, contractile function and response to EC

This can often be corrected by surgery or other methods