筋萎縮性側索硬化症マウスモデルにおける水素富化生理食塩水投与による疾患進行抑制効果
Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron disorder in which oxidative and nitrosative stress are implicated in pathogenesis. This animal study examined the effects of intraperitoneally administered hydrogen-rich saline (HRS) in SOD1 G93A transgenic mice. HRS-treated animals showed delayed symptom onset and extended survival compared with controls. Motor neuron loss was reduced, and microglial as well as glial activation was suppressed. Mitochondrial apoptogenic factor release and downstream caspase-3 activation were inhibited by HRS. Markers of oxidative damage—including protein carbonyl, 3-nitrotyrosine, reactive oxygen species, peroxynitrite, and malondialdehyde—were all decreased. Mitochondrial function was preserved, evidenced by restored Complex I and IV activities, reduced mitochondrial ROS, and enhanced ATP synthesis. These findings suggest that molecular hydrogen exerts neuroprotective effects in ALS, likely through attenuation of oxidative/nitrosative stress and maintenance of mitochondrial integrity.
Molecular hydrogen scavenges ROS and peroxynitrite, restores mitochondrial Complex I and IV activities, suppresses release of apoptogenic factors, and inhibits caspase-3 activation, thereby protecting motor neurons from oxidative and nitrosative damage.
Intravenous hydrogen-saline infusion is a clinic-only route and is not viable for everyday self-administration. For routine hydrogen intake, inhalation is the most practical route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration 66% / 100% devices are not recommended).
See also:
https://h2-papers.org/en/papers/26537817