水素分子に対する生体応答と炎症性疾患への予防的効果
Molecular hydrogen (H₂) was long regarded as biologically inert in multicellular organisms due to the absence of hydrogenase. Research demonstrated that H₂ inhalation substantially reduces brain damage from focal ischemia-reperfusion by counteracting oxidative stress. Although H₂ reacts with hydroxyl radicals at a rate two to three orders of magnitude lower than conventional antioxidants, it was shown to react with Fenton reaction-derived hydroxyl radicals at room temperature without a catalyst, a property exploited in ophthalmic surgery. The anti-inflammatory actions of H₂ extend beyond reactive oxygen species scavenging; H₂ administration induces mild mitochondrial oxidative stress and activates Nrf2, a phenomenon termed mitohormesis, whereby sublethal mitochondrial stress confers cellular resilience. Crosstalk between antioxidative and anti-inflammatory signaling pathways, together with immune system modulation, is proposed as the central protective mechanism. Identifying the primary biomolecular target of H₂ is highlighted as a key objective for advancing its medical applications.
H₂ scavenges Fenton reaction-derived hydroxyl radicals and simultaneously induces mild mitochondrial oxidative stress, activating Nrf2 via mitohormesis. Crosstalk between antioxidative and anti-inflammatory pathways, along with immune system regulation, underlies its cytoprotective effects.
This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/32981496