分子状水素はミトコンドリア複合体Iにおけるスーパーオキシド産生を抑制しミトコンドリア膜電位を低下させる
Using isolated mitochondria and cultured cells, this study examined how molecular hydrogen (H2) influences the mitochondrial energy-converting system. Addition of 25 µM H2 induced reverse electron transport (RET) even without succinate, shifting NADH levels from +0.0313 ± 0.0106 µM to +1.20 ± 0.302 µM. When 5 µM NADH was present, succinate-driven RET was converted to forward electron transport (FET), accompanied by a 51.1% reduction in superoxide generated predominantly at complex I. H2 alone decreased mitochondrial membrane potential by 11.3% in cultured cells, as measured by TMRE fluorescence. The findings suggest H2 acts as a regulator of electron flow direction in a NAD/NADH ratio-dependent manner, and may additionally neutralize semiquinone radicals to limit complex III-derived superoxide, thereby mitigating mitochondrial oxidative damage.
H2 modulates electron transport direction in a NAD/NADH ratio-dependent manner, suppressing complex I-derived superoxide by 51.1% and potentially neutralizing semiquinone radicals to reduce complex III superoxide output, while also lowering mitochondrial membrane potential.
This is basic research at the cellular or molecular level. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/31810604