水素水がSHR.Cg-Leprcp/NDmcrラット腎臓におけるグルコースおよびα,β-ジカルボニル化合物誘発性活性酸素産生に及ぼす抑制効果
In type 2 diabetes and metabolic syndrome, α,β-dicarbonyl compounds and advanced glycation end products drive renal reactive oxygen species (ROS) accumulation, contributing to kidney dysfunction. This study examined whether hydrogen-rich water (HRW) could reduce such ROS generation both in isolated kidney homogenates from Wistar rats and in a living metabolic syndrome model. In vitro incubation with HRW attenuated glucose- and α,β-dicarbonyl-induced ROS levels. In the SHR.Cg-Leprcp/NDmcr rat model, 16 weeks of HRW administration reduced renal ROS production by 34%. Renal concentrations of glyoxal, methylglyoxal, and 3-deoxyglucosone fell by 81%, 77%, and 60%, respectively. Significant positive correlations were identified between renal ROS levels and both glyoxal (r = 0.659, p = 0.008) and methylglyoxal (r = 0.782, p = 0.001) concentrations, suggesting that HRW limits dicarbonyl compound accumulation and consequent oxidative burden in the kidney.
HRW reduces the accumulation of α,β-dicarbonyl compounds—glyoxal, methylglyoxal, and 3-deoxyglucosone—in renal tissue, thereby limiting the ROS generation that these compounds induce, as confirmed by significant correlations between dicarbonyl and ROS levels.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/22776773