水素ガス吸入による虚血再灌流性肝障害への酸化ストレス軽減効果
Using a murine hepatic ischemia/reperfusion model, the portal triad supplying the left and left-middle liver lobes was fully occluded for 90 minutes, followed by 180 minutes of reperfusion. Administration of 1–4% H2 gas by inhalation during the final 190 minutes of this protocol resulted in marked reduction of hepatocyte death, along with decreased serum alanine aminotransferase levels and lower hepatic malondialdehyde concentrations, both indicators of oxidative tissue damage. Helium gas administered under identical conditions produced no comparable protection, confirming that the observed benefit is specific to molecular hydrogen. These findings suggest that H2 inhalation selectively neutralizes cytotoxic reactive oxygen species, particularly hydroxyl radicals, and may represent a broadly applicable approach for mitigating oxidative stress in organ injury contexts.
Inhaled molecular hydrogen selectively scavenges cytotoxic reactive oxygen species, including hydroxyl radicals, thereby reducing lipid peroxidation (malondialdehyde) and hepatocyte death during ischemia/reperfusion.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/17673169