Hydrogen in Drinking Water Reduces Dopaminergic Neuronal Loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Parkinson’s Disease

Abstract

It has been shown that molecular hydrogen (H2) acts as a therapeutic antioxidant and suppresses brain injury by buffering the effects of oxidative stress. Chronic oxidative stress causes neurodegenerative diseases such as Parkinson’s disease (PD). Here, we show that drinking H2-containing water significantly reduced the loss of dopaminergic neurons in PD model mice using both acute and chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The concentration-dependency of H2 showed that H2 as low as 0.08 ppm had almost the same effect as saturated H2 water (1.5 ppm). MPTP-induced accumulation of cellular 8-oxoguanine (8-oxoG), a marker of DNA damage, and 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation were significantly decreased in the nigro-striatal dopaminergic pathway in mice drinking H2-containing water, whereas production of superoxide (O2N2) detected by intravascular injection of dihydroethidium (DHE) was not reduced significantly. Our results indicated that low concentration of H2 in drinking water can reduce oxidative stress in the brain. Thus, drinking H2-containing water may be useful in daily life to prevent or minimize the risk of life style-related oxidative stress and neurodegeneration.

Study details

Article type

Original Research

Disease / injury model

1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease

Duration

35 days

Dose comparison

The study tested four concentrations of hydrogen in water (0.04, 0.08, 0.5, 1.5 ppm) and found that as low as 0.08 ppm was as effective as saturated hydrogen water (1.5 ppm) in reducing dopaminergic neuronal loss.

Dose-dependent effect

Yes

Outcome

Positive

Findings

Drinking hydrogen-containing water significantly reduced the loss of dopaminergic neurons in both acute and chronic MPTP mouse models of Parkinson’s disease. The neuroprotective effect was observed even at low concentrations of hydrogen (0.08 ppm), and was associated with decreased markers of DNA damage (8-oxoG) and lipid peroxidation (4-HNE), but not with a significant reduction in superoxide production. Behavioral impairment in the chronic model was also partially improved.