分子状水素の治療効果：ミトコンドリア複合体Ⅰを介した新たな作用機序の考察
This review examines a mechanistic framework for molecular hydrogen (H2) activity in mammalian cells that extends beyond its established role as a scavenger of hydroxyl radicals and peroxynitrite. H2, being nonpolar and neutral, distributes rapidly throughout the body via passive diffusion following administration. The review proposes that H2 may serve as both an electron and proton donor within the ubiquinone-binding chamber of mitochondrial complex I, a structure sharing evolutionary ties with membrane-bound [NiFe]-hydrogenases. Under pathological conditions—particularly during reoxygenation after hypoxia—excess electron accumulation drives reactive oxygen species (ROS) generation; H2 is proposed to rectify this disordered electron flow. Additionally, H2 may facilitate the full reduction of quinone intermediates to ubiquinol, thereby expanding the antioxidant capacity of the quinone pool and limiting ROS formation.
H2 is proposed to act as an electron and proton donor at the ubiquinone-binding site of mitochondrial complex I, correcting pathological electron accumulation during reoxygenation after hypoxia, reducing ROS generation, and converting quinone intermediates to fully reduced ubiquinol to enhance antioxidant capacity.
The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/31057105