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 (O2•−) 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.

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To understand the contribution of spacer structure toward electron transfer (ET) and to regulate electronic coupling between a redox pair, porphyrin−spacer−benzoquinone molecules were prepared where spacers are trans-decalin and dihalosubstituted tricyclo[4.4.1.0]undecane including a three-membered ring. These compounds were designed to have almost the same separation distance between a redox pair, the same number of intervening bonds, and the nearly equal free energy change associated with the ET reaction. The ET rates for the charge separation process were evaluated on the basis of the fluorescence lifetimes. A quite large difference in the ET rates was observed among these compounds, and the ET rates for the compounds having the three-membered rings were ca. 50 to 60 times larger than that with trans-decalin spacer in THF. From the analysis of temperature dependence of the ET rates, it was shown that the observed rate acceleration is caused by both an increase of the electronic coupling and a decrease of the reorganization energy. Ab initio calculations of the electronic coupling elements and on molecular orbitals for the cyclopropanes predicted that the former may be due to the enhancement of the ET pathways arising from the bent geometry of the spacer or of the mixing pathway induced by a very low lying antibonding orbital in the dihalosubstituted cyclopropane.