Hydrogen Water Failed to Protect Against Eye Disease in Mice Study
- Authors
- Qian Zhang, Ye Tao, Zuo-Ming Zhang
- Journal
- Life Sciences
- Year
- 2016
- DOI
- 10.1016/j.lfs.2016.04.015
- Study Type
- Mouse
- Outcome
- Neutral
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Oxygen-Induced Retinopathy
- Body System
- Visual System
TL;DR
Hydrogen-rich saline (HRS) did not prevent abnormal blood vessel growth in a mouse model of retinal damage caused by high oxygen levels and may actually promote such growth in normal retinas.
Key Finding
Hydrogen-rich saline at the tested dose failed to prevent retinal damage and abnormally promoted blood vessel growth in normal retinal development.
Summary
Researchers tested whether hydrogen-rich saline (a solution containing dissolved hydrogen gas) could protect against oxygen-induced retinopathy (abnormal blood vessel growth in the eye caused by excess oxygen) in mice. Contrary to expectations, the treatment did not reduce blood vessel leakage or abnormal vessel growth in the damaged retinas, and surprisingly, it actually increased abnormal blood vessel formation in normal, healthy retinas.
Practical Takeaway
This mouse study suggests hydrogen-rich saline may not be effective for oxygen-induced retinopathy and raises concerns about its safety in neonatal eye conditions. However, this is a single animal study, and results in mice do not always translate to humans; further research would be needed before drawing conclusions about hydrogen water use in people.
Abstract
Aims: Hydrogen-rich saline (HRS) is a novel protection against various oxidative disorders and almost all types of inflammation. Moreover, its toxicity and side effects are rarely reported. We sought to clarify the protective effect of HRS against the oxygen-induced retinopathy (OIR) in C57BL/6 J model. Main methods: The OIR in the HRS treated mice and the untreated controls were systematically compared. The retinas of both groups were analyzed using high-molecular-weight FITC-dextran staining of flat-mount preparations, hematoxylin and eosin (H&E) staining of cross-sections. The distribution and expression of the vascular endothelial growth factor (VEGF) were also evaluated by the immunohistochemical measurements between postnatal days 17 (P17) and P21. Key finding: The leakage and non-perfusion areas of retinal blood vessels were not alleviated in the HRS treatment group. Moreover, the number of preretinal vascular endothelial cell in the HRS treatment group was similar to that in the untreated group after exposure to hyperoxia (P>0.05). The degree of OIR was positively correlated with the expression level of VEGF. Intriguingly, the preretinal vascular endothelial cell count in the retinas of pups reared in room air with HRS treatment was 15.21±2.98. The preretinal vascular endothelial cell count of the HRS treated mice was significantly higher than that of the untreated group reared in room air. Significance: In summary, HRS therapy (at the dose of 10ml/day, applied between P12 and P17) did not inhibit retinal neovascularization in OIR; On the contrary, it would induce the retinal neovascularization during the development of normal retinas.