水素曝露による細胞内リン脂質の一過性増加とエネルギー代謝抑制の解析
Molecular hydrogen (H₂) exhibits antioxidant and anti-inflammatory properties, yet its underlying molecular mechanisms remain poorly characterized. This study investigated lipid compositional changes in SH-SY5Y neuroblastoma cells following 1-hour H₂ exposure using liquid chromatography–high-resolution mass spectrometry. Glycerophospholipid species—including phosphatidylethanolamine, phosphatidylinositol, and cardiolipin—showed transient increases. Metabolomic profiling simultaneously revealed a broad suppression of energy metabolism accompanied by reduced glutathione levels. Morphological examination of endosomes indicated structural alterations, and intracellular trafficking of cholera toxin B toward recycling endosomes near the Golgi apparatus was delayed in H₂-exposed cells. These findings suggest that H₂-driven lipid remodeling transiently depresses energy production and vesicular transport while concurrently elevating oxidative stress, potentially activating protective stress-response pathways.
H₂ exposure transiently elevates glycerophospholipids (phosphatidylethanolamine, phosphatidylinositol, cardiolipin), suppresses overall energy metabolism with concurrent glutathione reduction, and delays endosomal trafficking, collectively proposed to activate cytoprotective stress-response 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/36571379