December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Mechanisms of Sodium Nitroprusside-Induced Damage in the Chick Retina
Author Affiliations & Notes
  • WK Stell
    Cell Biology & Anatomy University of Calgary Calgary AB Canada
  • KJ BairdNeuroscience Research Group Lions Sight Centre
    Cell Biology & Anatomy University of Calgary Calgary AB Canada
  • Footnotes
    Commercial Relationships   W.K. Stell, None; K.J. Baird, None. Grant Identification: Stauffer Foundation (Toronto) and Gustus Sight Research Fund (University of Calgary)
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4530. doi:
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      WK Stell, KJ BairdNeuroscience Research Group Lions Sight Centre; Mechanisms of Sodium Nitroprusside-Induced Damage in the Chick Retina . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4530.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: In the chick eye, 100-200 nmol intravitreal sodium nitroprusside (SNP) releases nitric oxide (NO) which damages photoreceptors and retinal pigment epithelium (RPE) and induces inflammation (Baird & Stell, ARVO, 2001). NO can form peroxynitrite and damage cells by protein nitration and lipid peroxidation. Our purpose was to test whether SNP-induced damage is due to these reactions, and whether the damaging NO is derived directly from SNP or indirectly from cells of the immune system. Methods: 200 nmol SNP in 20µL saline was injected intravitreally into one eye of 7-day chicks. Some eyes were co-injected intravitreally or intraperitoneally with 200 nmol dexamethasone, an anti-inflammatory steroid. Dexamethasone was re-injected 2 and 4 days later. Saline was injected into contralateral control eyes. Eyes were removed 1, 3, or 7 days after initial injection, opened, paraformaldehyde-fixed, cryosectioned, and stained with 0.1% toluidine blue or labeled with antibodies to lipid peroxidation products malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE), and nitration product nitrotyrosine (NT), as well as rods, cones, and inducible nitric oxide synthase (iNOS). Results: SNP - At 1 day after injection of SNP, the RPE developed discontinuities and photoreceptor outer segments began to separate from it. Minimal immunoreactivity for MDA, HNE, NT, or iNOS was observed. At 3 days there was further damage, and maximal iNOS-immunoreactivity in Müller's cells, microglia, and some displaced amacrine cells. At 7 days the RPE and photoreceptors were mostly destroyed and no longer interdigitated. After 3 and 7 days, MDA- and HNE-immunoreactivity was seen in the RPE and photoreceptors, plus some HNE-label in the inner nuclear layer, and NT-immunoreactivity was seen in the inner nuclear layer, photoreceptor outer segments and debris. Dexamethasone - This agent had no effect on SNP-induced retinal damage. Dexamethasone-treated retinas were not immunoreactive for iNOS, and showed only minimal leukocyte infiltration. Conclusion: SNP damages RPE and photoreceptors by lipid peroxidation and peroxynitrite formation, presumably being reduced to release NO in these tissues. SNP causes a secondary immune response in retina and uvea, probably induced by substances released by damaged cells, but SNP-induced retinal damage does not require the immune response.

Keywords: 491 nitric oxide • 561 retinal degenerations: cell biology • 504 oxidation/oxidative or free radical damage 

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