title: Prevention of selenite-induced cataractogenesis by N-acetylcysteine in rats.
abstract: OBJECTIVE
  To evaluate the effect of N-acetylcysteine on selenite-induced cataract formation in a rat model.
  
  
  METHODS
  Thirty-four Sprague-Dawley rat pups were divided into three groups. Eight pups received only selenite on postpartum day 10 (group 1), 14 pups received selenite on day 10 and additional acetylcysteine on postnatal days 9 to 15 (group 2), and 12 pups received only saline (group 3, control). All pups were daily examined for the presence of cataract under the microscope, starting from the day their eyes opened. Glutathione and malondialdehyde levels were evaluated in both serum and lenticular samples while protein carbonyl level was studied only in lenticular samples.
  
  
  RESULTS
  In group 1, 50% of the rats developed dense nuclear opacities and 50% developed slight nuclear opacities, while in group 2 only 14.3% developed dense nuclear opacities and 21.4% developed slight nuclear opacities (p < 0.05). None of the rats in group 3 developed any lens opacity. In lenticular samples, mean glutathione level was statistically lower in group 1 compared to groups 2 and 3 (p < 0.05), while malondialdehyde and protein carbonyl levels were both statistically higher in group 1 compared to groups 2 and 3 (p < 0.05). Serum level of glutathione was statistically lower in group 1 compared to groups 2 and 3 (p < 0.05), while serum malondialdehyde level was statistically lower in group 3 compared to groups 1 and 2.
  
  
  CONCLUSIONS
  N-acetylcysteine appears to inhibit selenite-induced cataractogenesis in the rat model, and this seems to be caused by the prevention of oxidative damage.
authors.affiliation: Ophthalmology Department, Fatih University School of Medicine, Ankara, Turkey. baydunus@yahoo.com
authors.forename: Bahri
authors.initials: B
authors.lastname: Aydin
authors.forename: Ramazan
authors.initials: R
authors.lastname: Yagci
authors.forename: Fatma M
authors.initials: FM
authors.lastname: Yilmaz
authors.forename: Mesut
authors.initials: M
authors.lastname: Erdurmus
authors.forename: Remzi
authors.initials: R
authors.lastname: Karadağ
authors.forename: Ugurcan
authors.initials: U
authors.lastname: Keskin
authors.forename: Mustafa
authors.initials: M
authors.lastname: Durmus
authors.forename: Ramazan
authors.initials: R
authors.lastname: Yigitoglu
mesh_terms: D000111:Acetylcysteine / Q000627:therapeutic use*; D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000627:therapeutic use*; D002386:Cataract / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D050050:Protein Carbonylation / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018038:Sodium Selenite / Q000633:toxicity
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D008315:Malondialdehyde; D005978:Glutathione; D018038:Sodium Selenite; D000111:Acetylcysteine