Oxidative damage in ambulatory and non-ambulatory state in patients with Duchenne/Becker muscular dystrophy

Background Duchenne and Becker muscular dystrophies (DMD/BMD) are caused by mutations in DMD gene that codes for dystrophin and those mutations lead to skeletal muscle degeneration1, 2. It has been suggested a relation between oxidative damage with muscle function in DMD/DMB; however, there are few studies demonstrating this idea. We hypothesized there is a differential oxidative damage during progression of dystrophy. Objective To know the oxidative status in ambulatory and non-ambulatory patients with DMD/DMB. Methods We studied ambulatory (n=20) and non-ambulatory (n=8) DMD/BMD patients. Plasma concentration of total nitric oxide (NO), malondialdehyde (MDA) and thiol; DPPH scavenging % in plasma and NFκB mRNA in leukocytes were measured. Muscle damage was evaluated by functional scales. Results NO, MDA, and NFκB mRNA are increased in non-ambulatory boys, p
Journal of International Society of Antioxidants in Nutrition & Health, Vol 3, No 3 (2016)