David L L, Shearer T R
Toxicol Appl Pharmacol. 1984 Jun 15;74(1):109-15. doi: 10.1016/0041-008x(84)90276-x.
A dose of 20 mumol 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.
20微摩尔/千克体重的亚硒酸盐剂量是幼鼠白内障的强效且快速诱导剂。我们研究了亚硒酸盐的生理浓度在体外催化谷胱甘肽氧化的速率，发现亚硒酸盐是一种强巯基氧化剂。为了测试亚硒酸盐在体内是否有相同的作用，在给乳鼠注射致白内障剂量的亚硒酸盐后，测量了五种晶状体硫的氧化状态。测量包括还原型谷胱甘肽（GSH）、氧化型谷胱甘肽（GSSG）、蛋白结合型谷胱甘肽（PSSG）、还原型蛋白巯基（PSH）和氧化型蛋白巯基（PSSP）。虽然亚硒酸盐在注射后6天导致晶状体GSH降低了44%，但GSSG或PSSG均未同时增加。同样，也没有证据表明PSH氧化为PSSP增加。为了确定GSH的损失是否是亚硒酸盐性白内障的原因，我们给正常大鼠注射了谷胱甘肽合成抑制剂丁硫氨酸亚砜胺（BSO）。注射BSO后4天，晶状体GSH下降超过96%；然而，没有形成白内障。因此，亚硒酸盐性白内障似乎不是由广泛的巯基氧化引起的，也不能完全归因于GSH的损失。
