パーキンソン病に対する分子状水素吸入の作用機序と症例報告
In the midbrain of individuals with Parkinson's disease, hydroxyl radicals produced through the Fenton reaction initiate a cascade of dopamine oxidation. Because the hydrogen molecule is an exceptionally small diatomic species, it readily crosses cell membranes and reaches midbrain tissue, where it converts hydroxyl radicals into water, thereby interrupting dopamine oxidation. This paper examines the neurological etiology of Parkinson's disease from this mechanistic perspective and presents a case in which H2 inhalation was associated with symptomatic improvement, including reduction of postural bending and hand tremor. The authors propose that molecular hydrogen addresses fundamental obstacles encountered in central nervous system drug development, positioning it as a candidate approach for neurodegenerative conditions.
H2 molecules penetrate the blood-brain barrier and enter midbrain tissue, where they neutralize Fenton-reaction-derived hydroxyl radicals by converting them to water, thereby blocking the oxidative chain reaction that degrades dopamine.
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/39073335