Hydrogen Gas Protects Eye Cells from Damage in Lab Study

Authors
Journal
Clinical & Experimental Ophthalmology
Year
DOI
10.1111/ceo.12525
Study Type
Cell Culture
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Glaucoma
Body System
Visual System

TL;DR

Molecular hydrogen (H2) gas can protect eye cells from damage caused by harmful oxidative stress, which is linked to glaucoma.

Key Finding

Molecular hydrogen protected rat retinal cells from oxidative damage by reducing harmful peroxynitrite molecules, preventing cell death, and preserving mitochondrial function.

Summary

Researchers grew rat retina tissue in a lab and exposed it to a chemical that causes oxidative stress (cellular damage from harmful molecules called reactive oxygen species). When they added molecular hydrogen to the culture, it protected the retinal cells by reducing damage, preventing cell death, and maintaining the health of mitochondria (the cell's energy-producing structures). This suggests hydrogen might help prevent or treat glaucoma, a disease involving retinal damage.

Practical Takeaway

This is an early-stage laboratory study using rat tissue, not human trials, so it cannot yet demonstrate that hydrogen water would have these protective effects in people. The findings suggest hydrogen may warrant further investigation for potential eye health applications, but much more research—including human studies—would be needed before any clinical recommendations could be made.

Abstract

AbstractBackgroundOxidative and nitrative processes have an important role in the pathogenesis of glaucomatous neurodegeneration. Oxidative stress occurs when cellular production of reactive oxygen species outweighs the protective capacity of antioxidant defences. Reactive oxygen species are generated as by‐products of cellular metabolism, primarily in the mitochondria. Herein, we present a novel investigation of the effects of molecular hydrogen (H2) on retinal cells exposed to oxidative stress.MethodsWe cultured adult rat retinal tissues in an organotypic culture system with a nitric oxide donor, S‐nitroso‐N‐acetylpenicillamine, in the presence or absence of H2. Loss of mitochondrial membrane potential and apoptosis of retinal cells were analysed using a MitoTMRE detection kit and TdT‐mediated dUTP nick end labeling (TUNEL) assay, respectively. Tyrosine nitration levels and oxidative stress damage in the retina were evaluated using immunohistochemical staining. Retinal damage was quantified by measuring the numbers of cells in the ganglion cell and inner nuclear layers and the thickness of the retina.ResultsH2 suppressed loss of mitochondrial membrane potential and apoptosis in retinal cells. Moreover, H2 decreased the tyrosine nitration level and suppressed oxidative stress damage in retinal cells. S‐nitroso‐N‐acetylpenicillamine treatment decreased the cell numbers in the ganglion cell layer and inner nuclear layer, but the presence of H2 inhibited this reduction. These findings suggest that H2 has a neuroprotective effect against retinal cell oxidative damage, presumably by scavenging peroxynitrite.ConclusionsH2 reduces cellular peroxynitrite, a highly toxic reactive nitrogen species. Thus, H2 may be an effective and novel clinical tool for treating glaucoma and other oxidative stress‐related diseases.