クロルピリホスの亜慢性曝露によるラット肝毒性に対する水素分子の保護効果
This animal study examined whether 8-week oral intake of hydrogen-rich water (HRW) could mitigate liver damage in rats subjected to sub-chronic chlorpyrifos (CPF) exposure. CPF is an organophosphate insecticide associated with oxidative stress and hepatic dysfunction. Biochemical assays measuring SOD and CAT activity, along with GSH and MDA levels, were combined with histopathological and electron microscopy analyses. HRW intake restored SOD activity, reduced MDA levels, and improved liver function markers. PCR array analysis identified 12 oxidative stress-related genes with altered expression following CPF exposure; 8 of these, including the mitochondrial Sod2 gene, showed significant normalization with HRW intake. Electron microscopy further revealed that CPF-induced mitochondrial structural damage was reduced in HRW-treated animals. These findings suggest that oxidative stress signaling and mitochondrial pathways are involved in the hepatoprotective mechanism of molecular hydrogen.
Hydrogen-rich water selectively scavenges hydroxyl radicals, restoring SOD activity and reducing MDA levels. It normalizes expression of 8 oxidative stress-related genes including mitochondrial Sod2, and attenuates CPF-induced mitochondrial structural damage, implicating both oxidative stress signaling and mitochondrial pathways.
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/32955216