title: Hydrogen-rich water inhibits glucose and α,β -dicarbonyl compound-induced reactive oxygen species production in the SHR.Cg-Leprcp/NDmcr rat kidney.
abstract: BACKGROUND
  Reactive oxygen species (ROS) production induced by α,β-dicarbonyl compounds and advanced glycation end products causes renal dysfunction in patients with type 2 diabetes and metabolic syndrome. Hydrogen-rich water (HRW) increases the H2 level in blood and tissues, thus reducing oxidative stress in animals as well as humans. In this study, we investigated the effects of HRW on glucose- and α,β-dicarbonyl compound-induced ROS generation in vitro and in vivo.
  
  
  METHODS
  Kidney homogenates from Wistar rats were incubated in vitro with glucose and α,β-dicarbonyl compounds containing HRW, following which ROS levels were measured. In vivo animal models of metabolic syndrome, SHR.Cg-Leprcp/NDmcr rats, were treated with HRW for 16 weeks, following which renal ROS production and plasma and renal α,β-dicarbonyl compound levels were measured by liquid chromatograph mass spectrometer.
  
  
  RESULTS
  HRW inhibited glucose- and α,β-dicarbonyl compound-induced ROS production in kidney homogenates from Wistar rats in vitro. Furthermore, SHR.Cg-Leprcp/NDmcr rats treated with HRW showed a 34% decrease in ROS production. Moreover, their renal glyoxal, methylglyoxal, and 3-deoxyglucosone levels decreased by 81%, 77%, and 60%, respectively. Positive correlations were found between renal ROS levels and renal glyoxal (r = 0.659, p = 0.008) and methylglyoxal (r = 0.782, p = 0.001) levels.
  
  
  CONCLUSIONS
  These results indicate that HRW inhibits the production of α,β-dicarbonyl compounds and ROS in the kidneys of SHR.Cg-Leprcp/NDmcr rats. Therefore, it has therapeutic potential for renal dysfunction in patient with type 2 diabetes and metabolic syndrome.
authors: Department of Environmental Physiology, Shimane University Faculty of Medicine, Izumo, Shimane, 693-8501, Japan.
authors: Masanori
authors: M
authors: Katakura
authors: Department of Environmental Physiology, Shimane University Faculty of Medicine, Izumo, Shimane, 693-8501, Japan.
authors: Michio
authors: M
authors: Hashimoto
authors: Department of Environmental Physiology, Shimane University Faculty of Medicine, Izumo, Shimane, 693-8501, Japan.
authors: Yoko
authors: Y
authors: Tanabe
authors: Department of Environmental Physiology, Shimane University Faculty of Medicine, Izumo, Shimane, 693-8501, Japan.
authors: Osamu
authors: O
authors: Shido