title: Ascorbic acid protects the diaphragm muscle against myonecrosis in mdx mice.
abstract: OBJECTIVE
  Oxidative stress contributes to myonecrosis in the dystrophin-deficient fibers of mdx mice and in Duchenne's muscular dystrophy. We examined the effects of ascorbic acid (AA), an antioxidant and free radical scavenger, on the dystrophic diaphragm muscle.
  
  
  METHODS
  Mdx mice (14 d old) received AA for 14 d. Control mdx mice received saline. The muscle damage was visualized by the penetration of Evans blue dye into myofibers and the extent of inflammation was assessed by histologic analysis. Creatine kinase levels were measured for the biochemical evaluation of muscle fiber degeneration. The levels of tumor necrosis factor-α (a proinflammatory cytokine) and 4-hydroxynonenal (a marker of lipid peroxidation) were analyzed by immunoblotting.
  
  
  RESULTS
  Ascorbic acid decreased creatine kinase levels, myonecrosis, inflammation, and the levels of tumor necrosis factor-α and 4-hydroxynonenal.
  
  
  CONCLUSIONS
  The present results suggest that AA plays a protective role in dystrophic muscle degeneration, possibly by decreasing reactive oxygen species, and support further investigations of AA as a potential therapy for dystrophinopathies.
authors.affiliation: Departamento de Anatomia, Biologia Celular, Fisiologia e Biofísica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, São Paulo, Brazil.
authors.forename: Erika
authors.initials: E
authors.lastname: Tonon
authors.forename: Renato
authors.initials: R
authors.lastname: Ferretti
authors.forename: Jean Hideki
authors.initials: JH
authors.lastname: Shiratori
authors.forename: Humberto
authors.initials: H
authors.lastname: Santo Neto
authors.forename: Maria Julia
authors.initials: MJ
authors.lastname: Marques
authors.forename: Elaine
authors.initials: E
authors.lastname: Minatel
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000378:metabolism; D003964:Diaphragm / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D016189:Dystrophin / Q000172:deficiency; D005260:Female; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D051379:Mice; D018101:Mice, Inbred mdx; D018485:Muscle Fibers, Skeletal / Q000187:drug effects* / Q000473:pathology; D009136:Muscular Dystrophies / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009336:Necrosis / Q000517:prevention & control; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000447:Aldehydes; D000975:Antioxidants; D016189:Dystrophin; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D003402:Creatine Kinase; C027576:4-hydroxy-2-nonenal; D001205:Ascorbic Acid