Hydrogen Eye Drops Protect Retina from Damage in Animal Study
- Authors
- Hideaki Oharazawa, Tsutomu Igarashi, Takashi Yokota, Hiroaki Fujii, Hisaharu Suzuki, Mitsuru Machide, Hiroshi Takahashi, Shigeo Ohta, Ikuroh Ohsawa
- Journal
- Investigative Opthalmology & Visual Science
- Year
- 2010
- DOI
- 10.1167/iovs.09-4089
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Retinal Ischemia-Reperfusion Injury
- Body System
- Visual System
TL;DR
Hydrogen-infused eye drops can protect the retina from damage caused by temporary increases in eye pressure by reducing harmful oxidative stress.
Key Finding
Hydrogen-loaded eye drops reduced harmful free radicals in the retina and prevented cell death, with treated eyes recovering over 70% of normal retinal thickness after ischemia-reperfusion injury in rats.
Summary
Researchers tested whether hydrogen-enriched eye drops could protect rat retinas from damage caused by temporarily cutting off blood flow and then restoring it. When they applied these drops during and after the blood flow interruption, the hydrogen quickly reached the eye's interior, reduced harmful molecules called free radicals, and prevented the death of retinal cells. The treated eyes recovered more than 70% of their normal thickness, compared to untreated eyes.
Practical Takeaway
This rat study suggests hydrogen eye drops may have protective potential for retinal damage from blood flow interruption, but human testing is needed before any clinical use. The rapid penetration of hydrogen into the eye and lack of known toxicity are encouraging early signals, though the findings cannot yet be applied to human eye health.
Abstract
Purpose: Retinal ischemia-reperfusion (I/R) injury by transient elevation of intraocular pressure (IOP) is known to induce neuronal damage through the generation of reactive oxygen species. Study results have indicated that molecular hydrogen (H(2)) is an efficient antioxidant gas that selectively reduces the hydroxyl radical (*OH) and suppresses oxidative stress-induced injury in several organs. This study was conducted to explore the neuroprotective effect of H(2)-loaded eye drops on retinal I/R injury. Methods: Retinal ischemia was induced in rats by raising IOP for 60 minutes. H(2)-loaded eye drops were prepared by dissolving H(2) gas into a saline to saturated level and administered to the ocular surface continuously during the ischemia and/or reperfusion periods. One day after I/R injury, apoptotic cells in the retina were quantified, and oxidative stress was evaluated by markers such as 4-hydroxynonenal and 8-hydroxy-2-deoxyguanosine. Seven days after I/R injury, retinal damage was quantified by measuring the thickness of the retina. Results: When H(2)-loaded eye drops were continuously administered, H(2) concentration in the vitreous body immediately increased and I/R-induced *OH level decreased. The drops reduced the number of retinal apoptotic and oxidative stress marker-positive cells and prevented retinal thinning with an accompanying activation of Müller glia, astrocytes, and microglia. The drops improved the recovery of retinal thickness by >70%. Conclusions: H(2) has no known toxic effects on the human body. Thus, the results suggest that H(2)-loaded eye drops are a highly useful neuroprotective and antioxidative therapeutic treatment for acute retinal I/R injury.