水素水摂取による非アルコール性脂肪肝炎および関連肝発癌の進行抑制：マウスモデルを用いた検討
This mouse study examined whether hydrogen-rich water (HW) could limit the progression of nonalcoholic steatohepatitis (NASH) and related hepatocarcinogenesis, using a methionine-choline-deficient (MCD) diet model and STAM mice. Over 8 weeks, HW-fed mice showed reductions in plasma alanine aminotransferase, hepatic TNF-α and IL-6 expression, the oxidative stress marker 8-OHdG, and TUNEL-positive apoptotic cells compared with controls. Serum antioxidant capacity was greater in the HW group than in the pioglitazone group, although hepatic cholesterol reduction was less pronounced. In STAM mice, HW consumption was associated with significantly fewer hepatic tumors and smaller maximum tumor size relative to controls, suggesting that hydrogen-rich water may limit NASH-related oncogenesis through antioxidative and anti-inflammatory mechanisms.
Hydrogen-rich water selectively scavenges cytotoxic reactive oxygen species, thereby reducing hepatic oxidative stress markers (8-OHdG), pro-inflammatory cytokines (TNF-α, IL-6), and apoptosis, which collectively attenuate NASH progression and associated tumor development.
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/22505328