title: Functional and structural changes resulting from strain differences in the rat model of oxygen-induced retinopathy.
abstract: OBJECTIVE
  Results of studies that compared the racial incidence of retinopathy of prematurity (ROP) suggested that ocular pigmentation might offer protection against the development of severe ROP. The structural and functional consequences of postnatal hyperoxia (oxygen-induced retinopathy; OIR) were compared in albino Sprague-Dawley (SD) and pigmented Long-Evans (LE) rats to verify this finding.
  
  
  METHODS
  Newborn rats were exposed to 80% O(2) during selected postnatal day intervals. The severity of the OIR was determined by examining retinal flatmounts (retinal vasculature assessment), protein level quantification and cellular localization of fibroblast growth factor (FGF)-2 and ciliary neurotrophic factor (CNTF; Western blot analysis and immunohistochemistry, respectively), retinal histology, and photopic and scotopic electroretinograms (ERGs).
  
  
  RESULTS
  Irrespective of the parameter considered, structural and functional deficits resulting from postnatal hyperoxia were significantly more pronounced in LE rats. Although FGF-2 levels in LE rats had a tendency to increase after hyperoxia compared with normoxic littermates, it did not reach statistical significance. A similar finding was observed in SD rats. Of interest, however, baseline levels of FGF-2 were approximately four to five times higher in SD rats than in LE rats. There was a similar, hyperoxia-induced increase in CNTF levels between SD and LE rats.
  
  
  CONCLUSIONS
  The findings suggest an increased susceptibility of newborn LE rats to postnatal hyperoxia in comparison with SD rats. Whether a pro-oxidant rather than antioxidant role of melanin or other genetic factors can explain these differences in oxygen susceptibility of the animal model of this retinopathy, remains to be determined.
authors.affiliation: Department of Pharmacology and Therapeutics, University-Montreal Children's Hospital Research Institute, Montreal, Quebec, Canada.
authors.forename: Allison Lindsay
authors.initials: AL
authors.lastname: Dorfman
authors.forename: Anna
authors.initials: A
authors.lastname: Polosa
authors.forename: Sandrine
authors.initials: S
authors.lastname: Joly
authors.forename: Sylvain
authors.initials: S
authors.lastname: Chemtob
authors.forename: Pierre
authors.initials: P
authors.lastname: Lachapelle
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000235:genetics; D015153:Blotting, Western; D020934:Ciliary Neurotrophic Factor / Q000378:metabolism; D003623:Dark Adaptation; D004195:Disease Models, Animal; D004596:Electroretinography; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006801:Humans; D018496:Hyperoxia / Q000378:metabolism / Q000503:physiopathology*; D007150:Immunohistochemistry; D007231:Infant, Newborn; D008315:Malondialdehyde / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity; D051381:Rats; D020318:Rats, Long-Evans; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism / Q000503:physiopathology*; D015861:Retinal Neovascularization / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D012178:Retinopathy of Prematurity / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D020934:Ciliary Neurotrophic Factor; D016222:Fibroblast Growth Factor 2; D008315:Malondialdehyde; D010100:Oxygen