title: Molecular hydrogen alleviates motor deficits and muscle degeneration in mdx mice.
abstract: OBJECTIVE
  Duchenne muscular dystrophy (DMD) is a devastating muscle disease caused by a mutation in DMD encoding dystrophin. Oxidative stress accounts for dystrophic muscle pathologies in DMD. We examined the effects of molecular hydrogen in mdx mice, a model animal for DMD.
  
  
  METHODS
  The pregnant mother started to take supersaturated hydrogen water (>5 ppm) ad libitum from E15.5 up to weaning of the offspring. The mdx mice took supersaturated hydrogen water from weaning until age 10 or 24 weeks when they were sacrificed.
  
  
  RESULTS
  Hydrogen water prevented abnormal body mass gain that is commonly observed in mdx mice. Hydrogen improved the spontaneous running distance that was estimated by a counter-equipped running-wheel, and extended the duration on the rota-rod. Plasma creatine kinase activities were decreased by hydrogen at ages 10 and 24 weeks. Hydrogen also decreased the number of central nuclei of muscle fibers at ages 10 and 24 weeks, and immunostaining for nitrotyrosine in gastrocnemius muscle at age 24 weeks. Additionally, hydrogen tended to increase protein expressions of antioxidant glutathione peroxidase 1, as well as anti-apoptotic Bcl-2, in skeletal muscle at age 10 weeks.
  
  
  CONCLUSIONS
  Although molecular mechanisms of the diverse effects of hydrogen remain to be elucidated, hydrogen potentially improves muscular dystrophy in DMD patients.
authors: a Division of Neurogenetics , Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine , Japan.
authors: Satoru
authors: S
authors: Hasegawa
authors: a Division of Neurogenetics , Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine , Japan.
authors: Mikako
authors: M
authors: Ito
authors: b Department of Pathophysiological Laboratory Sciences , Nagoya University Graduate School of Medicine , Japan.
authors: Mayu
authors: M
authors: Fukami
authors: b Department of Pathophysiological Laboratory Sciences , Nagoya University Graduate School of Medicine , Japan.
authors: Miki
authors: M
authors: Hashimoto
authors: b Department of Pathophysiological Laboratory Sciences , Nagoya University Graduate School of Medicine , Japan.
authors: Masaaki
authors: M
authors: Hirayama
authors: a Division of Neurogenetics , Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine , Japan.
authors: Kinji
authors: K
authors: Ohno
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D016189:Dystrophin / Q000378:metabolism; D005260:Female; D006859:Hydrogen / Q000627:therapeutic use*; D051379:Mice; D008810:Mice, Inbred C57BL; D018101:Mice, Inbred mdx; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism; D020388:Muscular Dystrophy, Duchenne / Q000188:drug therapy* / Q000378:metabolism / Q000517:prevention & control; D018384:Oxidative Stress / Q000187:drug effects; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D016189:Dystrophin; D006859:Hydrogen
keywords: Duchenne muscular dystrophy; Molecular hydrogen; Muscle degeneration; Oxidative stress; mdx mouse