title: Cysteamine prevents the development of lens opacity in a rat model of selenite-induced cataract.
abstract: OBJECTIVE
  The activation of transglutaminase 2 (TG2) by oxidative stress through TGFβ has been reported to play a crucial role in cataract formation. The authors investigated whether TG2 is involved in selenite-induced cataract formation in rats and whether cysteamine, a chemical inhibitor of TG2, can prevent cataract formation in this model.
  
  
  METHODS
  Intracellular TG2 activity was monitored in a human lens epithelial cell (HLE-B3) line and cultured rat lenses after treatment with selenite. Rat pups (13 days old) were injected subcutaneously with sodium selenite (Na(2)SeO(3); 20 μmol/kg) and intraperitoneally with cysteamine (30, 40, and 60 mg/kg) for 14 days. Lenses were evaluated photographically at days 7 and 14. The concentrations of malondialdehyde and glutathione in the lenses were determined.
  
  
  RESULTS
  In HLE-B3 cells or rat lenses, selenite induced intracellular TG activity, which was inhibited by cysteamine. In selenite-treated rats, the rate of cataract formation was significantly reduced by cysteamine (P < 0.001). The mean cataract area in the lenses of cysteamine-treated rats was smaller than that of control rats (P < 0.01). The levels of total and reduced glutathione in the lenses of cysteamine-treated rats extracted at day 14 were higher than those of control rats.
  
  
  CONCLUSIONS
  Cysteamine suppresses cataract formation induced by selenite in rats, suggesting that cysteamine can be used as a pharmaceutical intervention to prevent or delay cataract formation.
authors.affiliation: Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Korea.
authors.forename: Sang-Mok
authors.initials: SM
authors.lastname: Lee
authors.forename: Eui Man
authors.initials: EM
authors.lastname: Jeong
authors.forename: Jinho
authors.initials: J
authors.lastname: Jeong
authors.forename: Dong-Myung
authors.initials: DM
authors.lastname: Shin
authors.forename: Hyun-Ju
authors.initials: HJ
authors.lastname: Lee
authors.forename: Hyo-Jun
authors.initials: HJ
authors.lastname: Kim
authors.forename: Jisun
authors.initials: J
authors.lastname: Lim
authors.forename: Jin-Haeng
authors.initials: JH
authors.lastname: Lee
authors.forename: Sung-Yup
authors.initials: SY
authors.lastname: Cho
authors.forename: Mee-Kum
authors.initials: MK
authors.lastname: Kim
authors.forename: Won-Ryang
authors.initials: WR
authors.lastname: Wee
authors.forename: Jin-Hak
authors.initials: JH
authors.lastname: Lee
authors.forename: In-Gyu
authors.initials: IG
authors.lastname: Kim
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002386:Cataract / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D002460:Cell Line; D003543:Cysteamine / Q000494:pharmacology*; D004195:Disease Models, Animal; D004789:Enzyme Activation; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D019204:GTP-Binding Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018038:Sodium Selenite; D011503:Transglutaminases / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D011837:Radiation-Protective Agents; C000717609:Tgm2 protein, rat; D003543:Cysteamine; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins; D005978:Glutathione; D018038:Sodium Selenite