水素水摂取が自然発症高血圧ラットの腎障害に及ぼす保護効果
This study examined the renal protective potential of hydrogen-rich water (HW; 1.3±0.2 mg/L) administered as drinking water for 3 months to spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto controls. Although blood pressure remained unchanged, HW consumption markedly reduced renal injury markers. Mechanistically, reactive oxygen species generation was suppressed, while the activities of superoxide dismutase, glutathione peroxidase, glutathione-S-epoxide transferase, and catalase were elevated, and NADPH oxidase activity was diminished. Pro-inflammatory cytokines—TNF-α, IL-6, IL-1β, and MCP-1—were downregulated, likely through inhibition of NF-κB activation. Mitochondrial function, including ATP synthesis and membrane integrity, was also preserved in HW-treated SHR. These findings suggest that hydrogen-rich water intake may serve as a supplementary approach to mitigate hypertension-associated renal damage.
Hydrogen-rich water scavenges reactive oxygen species, upregulates antioxidant enzymes (SOD, catalase, glutathione peroxidase), suppresses NADPH oxidase, and inhibits NF-κB-mediated inflammatory cytokine expression, collectively preserving mitochondrial ATP production and membrane integrity in hypertensive kidneys.
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/24652103