May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
Author Affiliations & Notes
  • L.K. Julian
    Servicio de Oftalmología, Hospital de Clínicas UBA, Buenos Aires, Argentina
  • E.M. López
    Facultad de Medicina, UBA, IBCyN Prof.E.De Robertis, Buenos Aires, Argentina
  • H. Coirini
    Conicet, IBYME, Buenos Aires, Argentina
  • J.J. López–Costa
    Facultad de Medicina, UBA, IBCyN Prof.E. De Robertis, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships  L.K. Julian, None; E.M. López, None; H. Coirini, None; J.J. López–Costa, None.
  • Footnotes
    Support  UBACYT–M047 and CONICET– PIP 819/98
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 783. doi:
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      L.K. Julian, E.M. López, H. Coirini, J.J. López–Costa; HIGH LEVELS OF GLUCOCORTICOIDS PARTICIPATE IN RETINAL DEGENERATION INDUCED BY CONTINUOUS ILLUMINATION. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):783.

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

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Abstract: : Purpose: Glucocorticoids (GC) exert a deletereous action on hippocampal CA3 neurons which may be avoided by surgical and pharmacological adrenalectomy.The oxidative stress produced by continuous illumination induces degeneration of photoreceptors. Our hypothesis is that this stressful exposure causes an increase of GC levels which could be involved in light induced retinal damage. The aim of the present work was to confirm this hypothesis. Methods: Sprague Dawley rats (n=15) were adrenalectomized under Ketamine anesthesia (50 mg/kg, IP) following ARVO Guidelines of Animal Use Statement. After 18 hs of recovery; adrenalectomized (ADX) and intact control animals (CTL) were submitted to continuous illumination (10000 lux) up to 7 days. Animals received water (CTL) or saline solution (ADX) and food ad libitum. Rats were anesthetized with chloral hydrate (350 mg/kg, IP) and sacrifized either before or after 1, 2, 5 and 7 days of continuous illumination. Eyes were removed and fixed by immersion in 4% paraformaldehyde solution. Cryostat sections were stained with hematoxiline–eosine and retinal thickness was determined with a Vidas image analyzer connected to an optical microscope. Data were statistically analyzed using the Student Newman–Keuls Multiple comparison test. Results: There were not differences between CTL and ADX retinas before illumination. After 24 hs of continuous illumination retinas of ADX rats were significantly thicker than CTL retinas (196.18±14.41 µm vs 129.97±19.34 µm, p<0.001). Picnotic nuclei were observed in the outer nuclear layer (ON) of CTL and ADX illuminated retinas. Photoreceptor segments were damaged in CTL retinas, but they were quite preserved in ADX retinas. After 7 days of illumination, an important degeneration of photoreceptors was observed in both, CTL and ADX rats. Cellular debris were observed between ON and retinal pigment epithelium (RPE), and vacuolar inclusions, compatible with lipofuscin, were detected in RPE. An important number of ON nuclei showed irregular boundaries and nuclear fragmentation compatible with apoptosis. However retinal thickness of ADX vs CTL rats was 73.36 ±12.62 µm vs 55.64 ±5.71 µm (p<0.001). Conclusions: The present results suggest that a high level of GC may be a collaborative factor in light induced retinal damage. The effect of GC must be taken in account in degenerative diseases of the retina.

Keywords: photoreceptors • degenerations/dystrophies • corticosteroids 

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