title: Intake of water with high levels of dissolved hydrogen (H2) suppresses ischemia-induced cardio-renal injury in Dahl salt-sensitive rats.
abstract: BACKGROUND
  Hydrogen (H(2)) reportedly produces an antioxidative effect by quenching cytotoxic oxygen radicals. We studied the biological effects of water with dissolved H(2) on ischemia-induced cardio-renal injury in a rat model of chronic kidney disease (CKD).
  
  
  METHODS
  Dahl salt-sensitive rats (7 weeks old) were allowed ad libitum drinking of filtered water (FW: dissolved H(2), 0.00 ± 0.00 mg/L) or water with dissolved H(2) produced by electrolysis (EW: dissolved H(2), 0.35 ± 0.03 mg/L) for up to 6 weeks on a 0.5% salt diet. The rats then underwent ischemic reperfusion (I/R) of one kidney and were killed a week later for investigation of the contralateral kidney and the heart.
  
  
  RESULTS
  In the rats given FW, unilateral kidney I/R induced significant increases in plasma monocyte chemoattractant protein-1, methylglyoxal and blood urea nitrogen. Histologically, significant increases were found in glomerular adhesion, cardiac fibrosis, number of ED-1 (CD68)-positive cells and nitrotyrosine staining in the contralateral kidney and the heart. In rats given EW, those findings were significantly ameliorated and there were significant histological differences between rats given FW and those given EW.
  
  
  CONCLUSIONS
  Consumption of EW by ad libitum drinking has the potential to ameliorate ischemia-induced cardio-renal injury in CKD model rats. This indicates a novel strategy of applying H(2) produced by water electrolysis technology for the prevention of CKD cardio-renal syndrome.
authors.affiliation: Division of Nephrology, Endocrinology and Vascular Medicine, Graduate School of Medicine, Tohoku University, Sendai, Japan. wanjun@med.tohoku.ac.jp
authors.forename: Wan-Jun
authors.initials: WJ
authors.lastname: Zhu
authors.forename: Masaaki
authors.initials: M
authors.lastname: Nakayama
authors.forename: Takefumi
authors.initials: T
authors.lastname: Mori
authors.forename: Keisuke
authors.initials: K
authors.lastname: Nakayama
authors.forename: Junichiro
authors.initials: J
authors.lastname: Katoh
authors.forename: Yaeko
authors.initials: Y
authors.lastname: Murata
authors.forename: Toshinobu
authors.initials: T
authors.lastname: Sato
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kabayama
authors.forename: Sadayoshi
authors.initials: S
authors.lastname: Ito
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D004572:Electrolysis; D006333:Heart Failure / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D006859:Hydrogen / Q000378:metabolism*; D007511:Ischemia / Q000150:complications*; D008297:Male; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D020303:Rats, Inbred Dahl; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D014867:Water / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D014867:Water; D006859:Hydrogen; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498911:Nox4 protein, rat