水素水はアセトアミノフェン誘発性肝毒性に対してマウスで保護効果を示す
This animal study examined the hepatoprotective capacity of hydrogen-rich water (HRW) in mice subjected to acetaminophen (APAP)-induced liver injury. At a lethal APAP dose of 750 mg/kg, the 5-day survival rate reached 60% in HRW-treated animals versus 26.67% in controls. Following a sub-lethal dose of 500 mg/kg, serum markers of hepatocellular damage—ALT, AST, alkaline phosphatase, total bilirubin, and lactate dehydrogenase—were significantly reduced in HRW-treated mice at 24, 48, and 72 hours. Histological analysis revealed smaller necrotic areas and lower liver index values. Oxidative stress indicators showed decreased malondialdehyde and elevated superoxide dismutase activity and glutathione content. Pro-inflammatory cytokines TNF-α and IL-6 were suppressed, and expression of 4-HNE, nitrotyrosine, phosphorylated JNK, connexin 32, and CYP2E1 was inhibited. Additionally, enhanced hepatocyte mitosis suggested accelerated liver regeneration in HRW-treated animals.
HRW reduces lipid peroxidation (MDA) while restoring SOD activity and glutathione levels, suppresses pro-inflammatory cytokines (TNF-α, IL-6), inhibits JNK phosphorylation and CYP2E1 expression, and promotes hepatocyte mitosis, collectively attenuating APAP-induced hepatocellular damage.
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/25892869