One of the toxic effects of selenite is the development of bilateral nuclear cataracts in suckling rats. These lesions can be induced by a single subcutaneous injection of sodium selenite. Several studies have shown some biochemical changes associated with the selenite-induced cataract1-3), but the mechanisms of selenite cataract formation are still unknown. Selenite is a strong sulfhydryl oxidant in vitro4) and the aggregation of lens proteins by disulfide cross-links has been show to play an important role in cataract formation5). A decrease in lens glutathione and a reduction in lens protein sulfhydryl have been reported in selenite-induced cataract1, 6). David and Shearer7) reported that during selenite-induced cataractogenesis, there was no decrease in lens protein sulfhydryl content, though the loss of glutathione did occur. They claimed that the selenite-induced cataract could not be attributed to the reduction of lens sulfhydryl levels. As described above, explanations for the mechanism of selenite-induced cataract are controversial. Therefore, the purpose of this study is to further clarify the role of sulfhydryl oxidation in the cataract induced by selenite. Our findings are that inhibition of glutathione synthesis in rat pups induced by the intraperitoneal (i.p.) administration of buthionine sulfoximine (BSO) increased the cataract incidence caused by a single subcutaneous (s.c.) injection of selenite; furthermore, selenite induced the decomposition of lens protein and the formation of disulfide-linked lens protein aggregates in vitro and in vivo. Our data suggest that the oxidation of lens protein sulfhydryl by selenite is associated with selenite-induced cataractogenesis.