Hydrogen Water Protects Eyes from Chemical Burns in Animal Study
- Authors
- Takeshi Arima
- Journal
- International Journal of Ophthalmology
- Year
- 2020
- DOI
- 10.18240/ijo.2020.08.01
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Chemical Eye Burns
- Body System
- Ocular
TL;DR
Treating rat eyes with hydrogen-infused saline after a chemical injury reduces inflammation and unwanted blood vessel growth by boosting the activity of a protective enzyme.
Key Finding
Hydrogen-infused saline increased the activity of a protective antioxidant enzyme (SOD1) to approximately 2.5-fold higher levels in chemically burned rat corneas while reducing inflammation and abnormal blood vessel growth.
Summary
Researchers tested whether hydrogen-infused saline could help rat corneas recover from chemical burns. They applied either regular saline or hydrogen-containing saline to burned corneas and measured inflammation, new blood vessel growth, and levels of an antioxidant enzyme called SOD1 (a protein that protects cells from damage). Hydrogen treatment reduced inflammatory cells and abnormal blood vessel growth, and increased SOD1 activity to about 2.5 times higher than in untreated corneas.
Practical Takeaway
This rat study suggests hydrogen may help protect corneal tissue from chemical injury by boosting natural antioxidant defenses, but this is early-stage research in animals only. Human studies would be needed to determine if hydrogen water or hydrogen-infused saline could have similar protective effects in people with eye injuries.
Abstract
Aim: To investigate the effects of hydrogen (H2) on Cu, Zn superoxide dismutase (SOD1) activation in a rat model of corneal alkali burn. Methods: In each rat, one cornea was subjected to alkali exposure. Physiological saline (saline group) or H2-dissolved saline (H2 group) was instilled continuously on the cornea for 5min before and after alkali exposure. Inflammatory cells, neovascularization, and cytoplasmic SOD1 levels were evaluated immunohistochemically in enucleated eyes from both groups. Three-dimensional ultrastructural tissue changes in the eyes were analyzed using low-vacuum scanning electron microscopy. Results: The numbers of both inflammatory and vascular endothelial cells were significantly reduced in the corneas of the H2 group (P<0.01). Furthermore, H2 treatment increased both cytoplasmic SOD1 levels (P<0.01) and activity in corneal epithelial cells (P<0.01). Notably, the SOD1 activity level in the H2 group was approximately 2.5-fold greater than that in the saline group. Conclusion: H2 treatment suppresses inflammation and neovascularization in the injured cornea and indirectly suppresses oxidative insult to the cornea by upregulating the SOD1 enzyme protein level and activity.