title: Termination of experimental galactosemia in rats, and progression of retinal metabolic abnormalities.
abstract: OBJECTIVE
  To investigate the effect of termination of galactose feeding after a very short duration of experimental galactosemia on the biochemical abnormalities that are postulated to contribute to the development of retinopathy.
  
  
  METHODS
  Experimentally galactosemic rats (normal rats fed a 30% galactose-rich diet for 2 months) were fed a galactose-free diet for an additional 1 month. At the end of 3 months, retinas were removed to measure oxidative stress, nitric oxides (NOs), activity of PKC, and levels of nitrotyrosine. Data were compared between rats in the control group (fed a normal diet) and those in the experimentally galactosemic group (30% galactose diet for the entire 3 months).
  
  
  RESULTS
  Interruption of 2 months of galactose feeding by withdrawal of galactose from the diet for 1 additional month had partially beneficial effects on retinal lipid peroxides, but the levels of an endogenous antioxidant, reduced glutathione (GSH), remained subnormal in the retina of galactose-withdrawal rats (P < 0.05 vs. normal and P > 0.05 vs. galactose group). Cessation of the galactose-rich diet had partially beneficial effects on NO levels in the retina, but the levels of nitrotyrosine, an indicator of the formation of peroxynitrite, and activation of PKC were not affected.
  
  
  CONCLUSIONS
  The results show that retinal dysmetabolism continues to progress after experimental galactosemia is terminated in rats: Particularly, antioxidant levels remain subnormal, and nitrotyrosine levels are elevated for at least 1 month. Identification of metabolic abnormalities associated with the progression of incipient retinopathy after hyperglycemia is normalized may help in the search for the cause of retinopathy.
mesh_terms: D000818:Animals; D018450:Disease Progression; D004334:Drug Administration Schedule; D005690:Galactose / Q000008:administration & dosage; D005693:Galactosemias / Q000139:chemically induced / Q000150:complications*; D005978:Glutathione / Q000378:metabolism; D006601:Hexoses / Q000097:blood; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008659:Metabolic Diseases / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D018384:Oxidative Stress; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000378:metabolism*; D012164:Retinal Diseases / Q000378:metabolism*; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000378:metabolism
chemical_list: D006601:Hexoses; D008054:Lipid Peroxides; C002744:3-nitrotyrosine; D014443:Tyrosine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D011493:Protein Kinase C; D005978:Glutathione; D005690:Galactose