酸化的リン酸化脱共役による急性腎障害モデルにおける水素飽和水利尿の腎保護効果
Using 60 nonlinear male rats (0.16–0.18 kg), this study examined how a hydrogen-rich solution (1.2 ppm H2, redox potential −297.3±5.27 mV) affects renal function under tissue hypoxia induced by 2,4-dinitrophenol (3 mg/kg), an uncoupler of oxidative phosphorylation. Functional, biochemical, histoenzymochemical, and immunoassay methods were applied. Administration of the hydrogen-saturated negative-redox-potential solution improved sodium ion reabsorption in the distal nephron, reduced tubular proteinuria, elevated succinate dehydrogenase activity in the proximal nephron, and shifted urinary redox potential toward negative values. Plasma concentrations of proinflammatory cytokines—TNF-α, IL-1β, and IL-6—were lowered, and oxidative protein modification in the renal cortex was attenuated. These findings indicate that molecular hydrogen exerts a protective influence on kidney tissue under hypoxic conditions associated with mitochondrial uncoupling.
Molecular hydrogen scavenges hydroxyl radicals and peroxynitrite, supplies additional electrons to mitochondria, and thereby reduces oxidative stress and proinflammatory cytokine levels, attenuating hypoxic renal injury caused by uncoupling of oxidative phosphorylation.
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/36567846