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Hydrogen prevents corneal endothelial damage in phacoemulsification cataract surgery
In phacoemulsification, ultrasound induces hydroxyl radical (·OH) formation, damaging corneal endothelium. Whether H 2 can prevent such oxidative damage in phacoemulsification was examined by in vitro and in vivo studies. H 2 was dissolved in a commercial irrigating solution. The effects of H 2 agai...
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Published in: | Scientific reports 2016-08, Vol.6 (1), p.31190-31190, Article 31190 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | In phacoemulsification, ultrasound induces hydroxyl radical (·OH) formation, damaging corneal endothelium. Whether H
2
can prevent such oxidative damage in phacoemulsification was examined by
in vitro
and
in vivo
studies. H
2
was dissolved in a commercial irrigating solution. The effects of H
2
against ·OH generation were first confirmed
in vitro
by electron-spin resonance (ESR) and hydroxyphenyl fluorescein (HPF). ESR showed a significantly decreased signal magnitude and fluorescence intensity by oxidized HPF was significantly less in the H
2
-dissolved solution. The effects of H
2
in phacoemulsification were evaluated in rabbits, comparing H
2
-dissolved and control solutions. Five hours after the procedure, the whole cornea was excised and subjected to image analysis for corneal edema, real-time semiquantitative PCR (qPCR) for heme oxygenase (HO)-1, catalase (CAT), superoxide dismutase 1 (SOD1) and SOD2 mRNA and immunohistochemistry. Corneal edema was significantly less and the increases in anti-oxidative HO-1, CAT and SOD2 mRNA expressions were significantly suppressed in the H
2
group. In addition, corneal endothelial cell expressions of two oxidative stress markers, 4-HNE and 8-OHdG, were significantly lower in the H
2
group. In conclusion, H
2
dissolved in the ocular irrigating solution protected corneal endothelial cells from phacoemulsification-induced oxidative stress and damage. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/srep31190 |