経口水素水投与によるラット腎移植後慢性拒絶反応（慢性移植腎症）の抑制
Reactive oxygen species (ROS) are implicated in the interstitial fibrosis and tubular atrophy characteristic of chronic allograft nephropathy (CAN). Using an orthotopic kidney transplantation model (Lewis-to-Brown Norway rat), animals received hydrogen-rich water (HW) or regular water from day 0 through day 150 post-transplant. Recipients given regular water progressively developed proteinuria and declining creatinine clearance, culminating in graft failure. By contrast, HW-treated animals maintained better allograft function, showed slower CAN progression, exhibited reduced oxidative damage and inflammatory mediator levels, and achieved higher overall survival rates. Activation of mitogen-activated protein kinase inflammatory signaling cascades was markedly lower in renal allografts from HW-treated animals. These findings indicate that orally administered molecular hydrogen exerts antioxidant and anti-inflammatory effects capable of preserving transplanted kidney function in this experimental model.
Molecular hydrogen scavenges ROS, thereby reducing oxidative damage and dampening MAPK-mediated inflammatory signaling, which collectively limits interstitial fibrosis and tubular atrophy in renal allografts.
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/19907413