慢性炎症性疾患における水素の可能性：ミトコンドリアストレス抑制を介したメカニズムの考察
Mitochondria are the primary intracellular source of reactive oxygen species (ROS), generating substantial quantities of the highly reactive hydroxyl radical (•OH). Molecular hydrogen (H2) can selectively neutralize •OH within mitochondria. Inflammatory responses are initiated by proinflammatory cytokines released from macrophages and neutrophils; however, dysregulated or excessive responses can culminate in acute or chronic inflammatory disease. Emerging evidence indicates that ROS activate NLRP3 inflammasomes, which in turn drive proinflammatory cytokine production. Although H2 has been shown to suppress mitochondrial ROS, the precise mechanism by which it may inhibit NLRP3 inflammasome activation through mitochondrial oxidation remains unclear. This review proposes a hypothetical mechanistic framework in which H2 attenuates mitochondrial oxidative stress, thereby reducing inflammasome-mediated inflammation. The authors discuss potential relevance to a range of chronic inflammatory conditions, including COVID-19.
H2 is proposed to selectively scavenge mitochondria-derived hydroxyl radicals, thereby suppressing ROS-dependent NLRP3 inflammasome activation and reducing downstream proinflammatory cytokine production.
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/33806292