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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 concentrationdependency

of H2 showed that H2 as low as 0.08 ppm had almost the same effect as saturated H2 water (1.5 ppm). MPTPinduced

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 stylerelated

oxidative stress and neurodegeneration.
 

Citation: Fujita K, Seike T, Yutsudo N, Ohno M, Yamada H, et al. (2009) 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. PLoS ONE 4(9): e7247. doi:10.1371/journal.pone.0007247

Editor: David C. Rubinsztein, University of Cambridge, United Kingdom

Received September 2, 2008; Accepted September 2, 2009; Published September 30, 2009

Copyright:  2009 Fujita et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits

unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: Supported by Panasonic Electric Works Co., Ltd., and Kyushu University Global COE program for NY, MO, KS, YN. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing Interests: The authors have declared that no competing interests exist.

* E-mail: noda@phar.kyushu-u.ac.jp

These authors contributed equally to this work.

 

 

 

 
 

 

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