Hydrogen Water Shows Promise for Protecting Vision in Retinal Disease
- Authors
- Tao Chen, Ye Tao, Weiming Yan, Guoqing Yang, Xuemin Chen, Ruidan Cao, Lei Zhang, Junhui Xue, Zuo-Ming Zhang
- Journal
- Experimental Eye Research
- Year
- 2016
- DOI
- 10.1016/j.exer.2016.05.017
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinitis Pigmentosa
- Body System
- Visual
TL;DR
A study found that injecting rats with hydrogen-rich saline could protect their eye cells from damage caused by a chemical that usually leads to a type of blindness.
Key Finding
Hydrogen-rich saline significantly reduced photoreceptor cell death and preserved retinal structure and function in rats with chemically-induced retinal degeneration, suggesting it may protect against oxidative stress damage in the eye.
Summary
Researchers tested hydrogen-rich saline (a solution containing dissolved hydrogen gas) as a potential treatment for retinitis pigmentosa, a disease that causes vision loss through the breakdown of light-sensing cells in the eye. In rats with chemically-induced retinal damage, hydrogen-rich saline reduced cell death, preserved the structure of damaged eye tissue, and improved electrical signals in the retina compared to untreated rats.
Practical Takeaway
While these results are promising, this is an early-stage animal study in rats, not humans. The findings suggest hydrogen-rich saline warrants further investigation as a potential treatment for retinitis pigmentosa, but much more research—including human clinical trials—would be needed before any therapeutic claims could be made.
Abstract
The N-methyl-N-nitrosourea (MNU)-treated rat is typically used as an animal model of chemically-induced retinitis pigmentosa (RP). Reactive oxygen species (ROS) have been recognized as the crucial contributor to the retinal photoreceptor apoptosis seen in MNU-treated rats. In the present study, we explored the therapeutic effects of hydrogen-rich saline (HRS), a selective ROS scavenger, on MNU-induced photoreceptor degeneration. Intraperitoneal (IP)administration of HRS ameliorated MNU-induced photoreceptor degeneration in terms of morphology and function: Sharply decreased thickness of the retinal outer nuclear layer (ONL) and flattened photopic and scotopic electroretinogram (ERG) waveforms, typically seen in response to MNU treatment, were substantially rescued in rats cotreated with MNU and HRS (MNU + HRS). Moreover, the terminal deoxyuridine triphosphate nick-end labeling (TUNEL) assay revealed a smaller number of apoptotic photoreceptors in the MNU + HRS group compared that in the MNU group. Compared to MNU-treated rats, retinal malondialdehyde (MDA) content in MNU + HRS rats significantly decreased while superoxide dismutase (SOD) activity significantly increased. Morphological and multi-electrode array (MEA) analyses revealed more efficient preservation of the architecture and field potential waveforms in particularly the peripheral regions of the retinas within the MNU + HRS group, compared to that in the MNU group. However, this enhanced protection of structure and function in the peripheral retina is unlikely the result of site-dependent variation in the efficacy of HRS; rather, it is most likely due to reduced susceptibility of peripheral photoreceptors to MNU-induced degeneration. Inner retinal neuron function in the MNU + HRS rats was better preserved, with fewer apoptotic photoreceptors in the ONL. Collectively, these results support the rationale for future clinical evaluation of HRS as a therapeutic agent for human RP.