December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Does Melanin Protect The Retina From Oxygen Toxicity?
Author Affiliations & Notes
  • AL Dorfman
    Pharmacology and Therapeutics
    McGill University Montreal PQ Canada
  • O Dembinska
    Ophthalmology & Neurology-Neurosurgery
    McGill University Montreal PQ Canada
  • S Joly
    Dép de biologie Univ de Montréal Montreal PQ Canada
  • J Racine
    Ophthalmology & Neurology-Neurosurgery
    McGill University Montreal PQ Canada
  • E Simard
    Montreal Children's Hospital Montreal PQ Canada
  • H Moukhles
    Dép de biologie Univ de Montréal Montreal PQ Canada
  • S Chemtob
    Pharmacology and Therapeutics
    McGill University Montreal PQ Canada
  • P Lachapelle
    Ophthalmology & Neurology-Neurosurgery
    McGill University Montreal PQ Canada
  • Footnotes
    Commercial Relationships   A.L. Dorfman, None; O. Dembinska, None; S. Joly, None; J. Racine, None; E. Simard, None; H. Moukhles, None; S. Chemtob, None; P. Lachapelle, None. Grant Identification: Support: FRSQ, CIHR, GRENE, Réseau Vision
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1785. doi:
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    • Get Citation

      AL Dorfman, O Dembinska, S Joly, J Racine, E Simard, H Moukhles, S Chemtob, P Lachapelle; Does Melanin Protect The Retina From Oxygen Toxicity? . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1785.

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

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Abstract

Abstract: : Purpose: Previous studies suggested that free radicals might play a role in retinopathy of prematurity (ROP) and melanin was previously shown to act as a free radical scavenger. The aim of this study was to investigate, using pigmented rats, whether melanin helps in preventing the structural and functional consequences of Oxygen Induced Retinopathy (OIR). Methods: Newborn pigmented Long-Evans (LE) and albino Sprague Dawley (SD) rats were exposed to 22.5 hours of 80% O2 interrupted by 3 periods of 0.5 hours at 21% O2. Rats were grouped at birth into seven exposure regimens; postnatal days 0-6, 0-9, 0-12, 0-14, 6-14, 9-14, 12-14 and one control group exposed to 21% O2 from day 0-14 (n=4 for each group). Scotopic (intensity:-6.3 to 0.6 log cd.m-2.sec; 12 hrs dark adaptation) and photopic (intensity:0.9 log cd.m-2.sec; background: 30cd.m-2) ERGs were recorded at 30 days. Results: After exposure to O2 in the first week of life (P0-6), the amplitude of the scotopic a-wave was attenuated to 90% of control in LE rats, while no change was observed in SD rats. Two-week exposure (P0-14) brought on a further attenuation to 50% of control in LE rats, compared to 20% in SD rats. Exposure to oxygen from P0-6 also attenuated the amplitude of the Rod Vmax b-wave of LE rats to 60% of control, compared to 95% in SD rats. Exposure from P0-14 caused for a further reduction in these values to 10% and 35%, respectively. In comparison, exposure from P0-6 caused the photopic b-wave to be reduced to 65% of control in LE as opposed to 85% in SD rats. Increasing the exposure regimen from P0-14 caused for a further attenuation to 15% and 25%, for LE and SD rats, respectively. Conclusions: Our results show that melanin, an endogenous free radical scavenger, did not prove to exert the predicted protective effect in OIR. Following postnatal oxygen exposure, LE rats were affected earlier on and more drastically than SD rats. These results support our previous demonstration that concurrent administration of Trolox C, a synthetic free radical scavenger, showed only a minimal protective effect. It therefore still remains important to determine the role played by free radicals in causing ROP. It was previously suggested (Dembinska et al., 2001) that the retina's susceptibility to oxygen toxicity varies as a function of the degree of retinal maturity reached at the time of exposure. Perhaps the retina develops differently in LE and SD rats, a feature that might explain the above discrepancies.

Keywords: 572 retinopathy of prematurity • 396 electroretinography: non-clinical 
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