酸化ストレス下のヒトケラチノサイトにおいて水素ガスがジスルフィド結合を還元することでIP3Rを保護する
Reactive oxygen species (ROS) generated by hydrogen peroxide (H₂O₂) are implicated in skin aging through oxidative modification of proteins, particularly via disulfide bond formation at cysteine and methionine residues. Using H₂O₂-treated human keratinocytes as a model of skin aging, this study found that H₂O₂ impaired ATP-induced Ca²⁺ signaling in a dose-dependent manner, linked to disulfide bond formation in inositol 1,4,5-trisphosphate receptors (IP3Rs). Co-treatment with β-mercaptoethanol partially restored Ca²⁺ responses by reducing these disulfide bonds. Molecular hydrogen (H₂) demonstrated superior protection of IP3R1 function compared with direct ROS scavenging, acting primarily through reduction of disulfide bridges rather than quenching oxidants. These findings suggest that ROS-driven disulfide bond formation in Ca²⁺-signaling proteins is a key mechanism in skin aging, and that H₂ can counteract this process.
H₂ protects IP3R1-mediated Ca²⁺ signaling primarily by reducing oxidative disulfide bonds formed at cysteine/methionine residues, rather than by directly scavenging ROS.
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/28620198