Abstract
A dose of 20 μmol selenite/kg body weight is a potent and a very rapid inducer of cataracts in young rats. We investigated the rate at which physiological concentrations of selenite would catalyze the oxidation of glutathione in vitro and found that selenite was a strong sulfhydryl oxidant. To test if selenite had the same effect in vivo, the oxidation state of five kinds of lenticular sulfur were measured in suckling rats following a cataractous dose of selenite. The measurements included reduced glutathione (GSH), oxidized glutathione (GSSG), protein-bound glutathione (PSSG), reduced protein sulfhydryl (PSH), and oxidized protein sulfhydryl (PSSP). While selenite caused a 44% decrease in lens GSH by 6 days postinjection, there was no concurrent increase in either GSSG or PSSG. Likewise, there was no evidence for increased oxidation of PSH to PSSP. To determine if GSH loss were the cause of the selenite cataracts, we injected normal rats with the glutathione synthesis inhibitor buthionine sulfoximine (BSO). Lens GSH dropped more than 96% by 4 days post-BSO injection; however, no cataracts formed. Thus, selenite cataract does not appear to be caused by extensive sulfhydryl oxidation and cannot be attributed exclusively to GSH loss.
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