Hydrogen Water Protects Eyes from Damage After Blood Flow Blockage
- Authors
- Hongwei Liu, Ning Hua, Keliang Xie, Tingting Zhao, Yong-Hao Yu
- Journal
- Molecular Medicine Reports
- Year
- 2015
- DOI
- 10.3892/mmr.2015.3731
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Retinal Ischemia-Reperfusion Injury
- Body System
- Nervous System
TL;DR
Hydrogen-rich saline may protect the retina from damage caused by temporary loss and restoration of blood supply by reducing DNA damage and cell death.
Key Finding
Hydrogen-rich saline reduced retinal cell death and DNA damage in rats with ischemia-reperfusion injury by inhibiting overactivation of PARP-1, a protein involved in programmed cell death.
Summary
Researchers tested whether hydrogen-rich saline could protect rat eyes from damage caused by temporarily cutting off blood flow and then restoring it (a condition called ischemia-reperfusion injury). They found that hydrogen-rich saline reduced cell death and damage in the retina by decreasing oxidative stress (harmful chemical reactions) in DNA and blocking overactivation of a protein called PARP-1 that triggers cell death.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen-rich saline may have protective effects against certain types of eye damage from blood flow disruption. However, this was conducted only in rats, and human studies would be needed to determine if these findings apply to people. The study does not provide evidence that hydrogen water would have similar effects.
Abstract
Overactivation of poly (ADP-ribose) polymerase 1 (PARP-1), as a result of sustained DNA oxidation in ischemia‑reperfusion injury, triggers programmed cell necrosis and apoptosis. The present study was conducted to demonstrate whether hydrogen‑rich saline (HRS) has a neuroprotective effect on retinal ischemia reperfusion (RIR) injury through inhibition of PARP‑1 activation. RIR was induced by transient elevation of intraocular pressure in rats. HRS (5 ml/kg) was administered peritoneally every day from the beginning of reperfusion in RIR rats until the rats were sacrificed. Retinal damage and cell death was determined using hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. DNA oxidative stress was evaluated by immunofluorescence staining of 8‑hydroxy‑2‑deoxyguanosine. In addition, the expression of PARP‑1 and caspase‑3 was investigated by western blot analysis and/or immunohistochemical staining. The results demonstrated that HRS administration improved morphological alterations and reduced apoptosis following RIR injury. Furthermore, the present study found that HRS alleviated DNA oxidation and PARP‑1 overactivation in RIR rats. HRS can protect RIR injury by inhibition of PARP‑1, which may be involved in DNA oxidative stress and caspase-3-mediated apoptosis.