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Sang-Mok Lee, Eui Man Jeong, Jinho Jeong, Dong-Myung Shin, Hyun-Ju Lee, Hyo-Jun Kim, Jisun Lim, Jin-Haeng Lee, Sung-Yup Cho, Mee-Kum Kim, Won-Ryang Wee, Jin-Hak Lee, In-Gyu Kim; Cysteamine Prevents the Development of Lens Opacity in a Rat Model of Selenite-Induced Cataract. Invest. Ophthalmol. Vis. Sci. 2012;53(3):1452-1459. doi: 10.1167/iovs.11-8636.
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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.
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 (Na2SeO3; 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.
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.
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.
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