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Free radicals in rabbit retina under ocular hyperpressure and functional consequences
A Muller1, S Pietri, M Villain
1Laboratoire de Physiologie Cellulaire, Université Montpellier I, France.
Experimental Eye Research
|April 1, 1997
Summary
High intraocular pressure causes retinal oxidative stress and functional changes due to oxygen-derived free radicals. Direct measurements confirm free radical generation during acute ischemia, explaining electroretinogram alterations.
Area of Science:
- Ophthalmology
- Neuroscience
- Biochemistry
Background:
- Ocular ischemia, induced by high intraocular pressure, is linked to retinal oxidative stress and functional impairment.
- The specific oxygen-derived free radicals and their generation mechanisms during ocular ischemia remain unclear.
Purpose of the Study:
- To identify and characterize oxygen-derived free radicals produced in the retina during and after high intraocular pressure-induced ischemia.
- To correlate free radical generation with retinal function alterations.
Main Methods:
- Electron spin resonance (ESR) spin trapping using 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO) in retinal microdialysates.
- ESR measurement of ascorbyl free radical-dimethyl sulfoxide (AFR-DMSO) complex to assess oxidative stress.
- Electroretinogram (ERG) recordings to evaluate retinal function.
Main Results:
- Superoxide dismutase-inhibitable DEPMPO/hydroxyl radical adducts were detected during the high intraocular pressure period.
- Oxidative stress levels, assessed by spin trapping and AFR-DMSO, did not increase during reperfusion.
- Free radical scavengers demonstrated functional protection against high intraocular pressure-induced ERG alterations.
Conclusions:
- Direct ESR measurements confirm the production of oxygen-derived free radicals in the retina during acute ischemia.
- This free radical generation is a likely cause of electroretinogram alterations observed under high intraocular pressure.
- The findings elucidate the biochemical mechanisms underlying retinal damage in ocular ischemia.