水素ガスはフリーラジカル連鎖反応依存的な酸化リン脂質メディエーターの生成を修飾することで遺伝子発現を調節する
This study investigated the mechanism by which H2 controls gene expression. In a cell-free chemical system, approximately 1% H2 gas (v/v) inhibited the autoxidation of linoleic acid driven by free radical chain reactions. When the major phospholipid PAPC was autoxidized in the presence or absence of H2, the resulting profile of oxidized phospholipid species differed between conditions. Cultured cells exposed to H2-modified oxidized phospholipid species showed attenuated Ca²⁺ signaling, and comprehensive microarray analysis revealed broad changes in gene expression. Within intact cultured cells, H2 suppressed free radical-mediated lipid peroxidation and normalized elevated intracellular Ca²⁺ levels, thereby modulating Ca²⁺-dependent transcriptional programs. These findings suggest that H2 influences gene expression through the Ca²⁺ signaling pathway by altering the spectrum of oxidized phospholipid mediators generated during free radical chain reactions.
H2 suppresses free radical chain reactions, altering the oxidized phospholipid (PAPC) species profile. This modification normalizes intracellular Ca²⁺ signaling, which in turn regulates Ca²⁺-dependent gene expression across multiple pathways.
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/26739257