水素富化水摂取がラット心筋ミトコンドリア機能およびコエンザイムQに与える影響の新たな分子メカニズム
This animal study investigated how hydrogen-rich water (HRW) consumption affects cardiac mitochondrial function and coenzyme Q (CoQ) status in rats. Following HRW administration, electron transport chain activity was enhanced, and ATP production driven by both Complex I and Complex II substrates increased. CoQ concentrations rose in plasma, myocardial tissue, and isolated mitochondria, while plasma malondialdehyde—a marker of lipid peroxidation—declined. Based on these findings, the authors propose a novel metabolic mechanism in which molecular hydrogen acts as both an electron and proton donor within the mitochondrial Q-cycle, promoting the reduction of ubiquinone to ubiquinol. This shift suppresses lipid peroxidation and facilitates electron flow from Complexes I and II to Complex III, thereby augmenting oxidative phosphorylation and ATP synthesis. The results suggest that H2 may support myocardial energy metabolism by modulating CoQ redox status and mitochondrial respiratory chain efficiency.
Molecular hydrogen is proposed to donate both electrons and protons within the mitochondrial Q-cycle, reducing ubiquinone to ubiquinol. This increases CoQ availability, enhances electron transfer from Complexes I and II to Complex III, and boosts ATP production via oxidative phosphorylation while reducing lipid peroxidation.
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/31536712