Hydrogen Gas Protects Brain Cells from Damage and Death
- Authors
- Yayoi Murakami, Masafumi Ito, Ikuroh Ohsawa
- Journal
- PLoS One
- Year
- 2017
- DOI
- 10.1371/journal.pone.0176992
- Study Type
- Cell Culture
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Neurodegenerative Diseases
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas or drinking hydrogen-rich water can protect the brain from damage by boosting energy production and the cell's defense system against stress.
Key Finding
Molecular hydrogen protected brain cells from oxidative stress-induced death when given as a pretreatment, working through both direct antioxidant action and by activating the cells' natural defense systems.
Summary
This laboratory study examined how molecular hydrogen (H2) protects brain cells from damage caused by oxidative stress (a harmful chemical imbalance in cells). Researchers treated cultured human brain cells with hydrogen gas and then exposed them to a damaging chemical. They found that hydrogen pretreatment protected cells from death by working in two ways: directly neutralizing harmful molecules and triggering the cells to produce their own protective enzymes.
Practical Takeaway
This is an early-stage laboratory study in cultured cells, not humans or animals, so its relevance to hydrogen water consumption remains unclear. The findings suggest hydrogen may help cells resist damage, but much more research—including animal and human studies—would be needed before drawing conclusions about health benefits for neurodegenerative disease prevention.
Abstract
Inhalation of molecular hydrogen (H2) gas ameliorates oxidative stress-induced acute injuries in the brain. Consumption of water nearly saturated with H2 also prevents chronic neurodegenerative diseases including Parkinson's disease in animal and clinical studies. However, the molecular mechanisms underlying the remarkable effect of a small amount of H2 remain unclear. Here, we investigated the effect of H2 on mitochondria in cultured human neuroblastoma SH-SY5Y cells. H2 increased the mitochondrial membrane potential and the cellular ATP level, which were accompanied by a decrease in the reduced glutathione level and an increase in the superoxide level. Pretreatment with H2 suppressed H2O2-induced cell death, whereas post-treatment did not. Increases in the expression of anti-oxidative enzymes underlying the Nrf2 pathway in H2-treated cells indicated that mild stress caused by H2 induced increased resistance to exacerbated oxidative stress. We propose that H2 functions both as a radical scavenger and a mitohormetic effector against oxidative stress in cells.