騒音性難聴に対する分子状水素吸入の保護効果：モルモットを用いた検討
Noise-induced hearing loss is closely linked to reactive oxygen species generation in the cochlea, yet effective systemic drug delivery to the inner ear remains clinically challenging. This animal study investigated whether a single 1-hour inhalation of 2% molecular hydrogen (H2), administered immediately after 2 hours of broadband noise exposure, could protect cochlear structures in guinea pigs. Animals were assigned to six groups and assessed immediately, at 1 week, or at 2 weeks post-exposure using frequency-specific auditory brainstem response (ABR) measurements. At the 2-week time point, H2-treated animals showed significantly lower ABR thresholds compared with air-treated controls, along with marked preservation of outer hair cells throughout the cochlea. Quantification of synaptophysin immunoreactivity indicated that H2 inhalation also protected synaptic structures of inner hair cells. Conversely, an elevated Iba1 signal in the stria vascularis suggested a heightened local inflammatory response in H2-treated animals. The authors note that repeated H2 inhalation sessions may yield greater benefit, and that translation to human clinical conditions requires further investigation.
H2 inhalation is proposed to selectively scavenge cochlear reactive oxygen species generated by noise exposure, thereby reducing oxidative damage to outer hair cells and inner hair cell synaptic structures and limiting auditory threshold shifts.
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/34140880