Systemic administration of phenyl-N-tert-butylnitrone protects the retina from light damage

Citation
I. Ranchon et al., Systemic administration of phenyl-N-tert-butylnitrone protects the retina from light damage, INV OPHTH V, 42(6), 2001, pp. 1375-1379
Citations number
38
Categorie Soggetti
da verificare
Journal title
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
ISSN journal
01460404 → ACNP
Volume
42
Issue
6
Year of publication
2001
Pages
1375 - 1379
Database
ISI
SICI code
0146-0404(200105)42:6<1375:SAOPPT>2.0.ZU;2-C
Abstract
PURPOSE. This study was conducted to test the hypothesis that phenyl-N-tert -butylnitrone (PBN), a spin-trapping agent known to cross the blood-brain b arrier and protect the brain from ischemia-reperfusion injury, is incorpora ted into the retina after intraperitoneal injection and protects photorecep tor cells from the damaging effects of constant visible light. METHODS. Albino rats were injected intraperitoneally with PEN (aqueous solu tion) or water, or were not injected, and then were placed in constant ligh t (2700 lux) for 24 hours. The incorporation of PEN into the retina was det ermined by highperformance liquid chromatography. Electroretinograms (ERGs) were recorded before light treatment and 1 and 15 days after the cessation of exposure to constant light. Eyes were taken for histology at each time point and outer nuclear layer (ONL) thickness determined. RESULTS. PBN was incorporated into the retina after intraperitoneal injecti on. Both control (water-injected and uninjected) groups exposed to constant light maintained only 28% of ONL thickness and 20% of retinal function, co mpared with the unexposed control group. In contrast, the PEN-treated anima ls maintained 80% of ONL thickness and exhibited 87% of retinal function. CONCLUSIONS. PBN protects the albino rat retina from the damaging effects o f constant light stress. That light-induced and hereditary retinal degenera tions share certain morphologic hallmarks and follow a similar apoptotic me chanism of degeneration raises the possibility of pharmacologic therapy for hereditary and environmentally induced neurodegenerative disorders.