Hydrogen Therapy Protects Eye Cells from Damage in Guinea Pig Study
- Authors
- Lihua Wei, Li Ge, Shucun Qin, Yunzhi Shi, Changqing Du, Hui Du, Liwei Liu, Yang Yu, Xue-Jun Sun
- Journal
- Experimental Eye Research
- Year
- 2012
- DOI
- 10.1016/j.exer.2011.11.016
- Study Type
- Guinea Pig
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinal Excitotoxicity
- Body System
- Visual System
TL;DR
Injecting hydrogen-rich saline into guinea pigs reduces eye damage caused by a harmful substance called glutamate.
Key Finding
Hydrogen-rich saline reduced retinal cell loss and preserved retinal structure in guinea pigs with glutamate-induced eye damage, with the greatest protection achieved when administered both directly into the eye and into the abdominal cavity.
Summary
Researchers tested whether hydrogen-rich saline could protect the retina (light-sensitive tissue at the back of the eye) from damage caused by excess glutamate, a chemical that can harm nerve cells. In guinea pigs with induced retinal injury, hydrogen-rich saline reduced cell death in the retina, preserved the retina's structure, and decreased markers of cellular stress. The treatment worked best when injected in two locations: directly into the eye and into the abdominal cavity.
Practical Takeaway
This animal study suggests hydrogen-rich saline may have potential to protect against certain types of retinal damage, but these results are from guinea pigs only and do not yet indicate whether the treatment would work in humans. Much more research, including human trials, would be needed before any health claims could be made about hydrogen water for eye health.
Abstract
Molecular hydrogen (H(2)) is an efficient antioxidant that can selectively reduce hydroxyl radicals and inhibit oxidative stress-induced injuries. We investigated the protective effects and mechanism of hydrogen-rich saline in a glutamate-induced retinal injury model. Retinal excitotoxicity was induced in healthy guinea pigs by injecting glutamate into the vitreous cavity. After 30 min, hydrogen-rich saline was injected into the vitreous cavity, the peritoneal cavity or both. Seven days later, the retinal stress response was evaluated by examining the stress biomarkers, inducible nitric-oxide synthase (iNOS) and glucose-regulated protein 78 (GRP78). The impaired glutamate uptake was assessed by the expression of the excitatory amino acid transporter 1(EAAT-1). The retinal histopathological changes were investigated, focusing on the thicknesses of the entire retina and its inner layer, the number of cells in the retinal ganglion cell layer (GCL) and the ultrastructure of the retinal ganglion cells (RGCs) and glial cells. Compared with the glutamate-induced injury group, the hydrogen-rich saline treatment reduced the loss of cells in the GCL and thinning of the retina and attenuated cellular morphological damage. These improvements were greatest in animals that received H(2) injections into both the vitreous and the peritoneal cavities. The hydrogen-rich saline also inhibited the expression of glial fibrillary acidic protein (GFAP) in Müller cells, CD11b in microglia, and iNOS and GRP78 in glial cells. Moreover, the hydrogen-rich saline increased the expression of EAAT-1. In conclusion, the administration of hydrogen-rich saline through the intravitreal or/and intraperitoneal routes could reduce the retinal excitotoxic injury and promote retinal recovery. This result likely occurs by inhibiting the activation of glial cells, decreasing the production of the iNOS and GRP78 and promoting glutamate clearance.