Calvin H I, Medvedovsky C, Worgul B V
Science. 1986 Aug 1;233(4763):553-5. doi: 10.1126/science.3726547.
The specific inhibitor of glutathione biosynthesis, L-buthionine sulfoximine (L-BSO), although relatively nontoxic in adult mice, induces severe glutathione depletion and age-specific pathological changes when repeatedly administered to male suckling mice. Dense cataracts developed when mice aged 9 to 12 days were given a series of injections of L-BSO, despite excellent survival and the absence of other significant long-term effects. By contrast, similar treatment of mice aged 14 to 17 days, although slightly less effective in reducing glutathione levels, resulted frequently in death, hind-leg paralysis, or impaired spermatogenesis, but did not produce cataracts. Administration of L-BSO to preweanling mice provides a novel model system for the induction of cataracts by depletion of lens glutathione and may enable the study of critical functions of glutathione in the lens and other growing tissues during early postnatal development.
谷胱甘肽生物合成的特异性抑制剂L-丁硫氨酸亚砜胺（L-BSO），尽管在成年小鼠中相对无毒，但当反复给予雄性乳鼠时，会导致严重的谷胱甘肽耗竭和年龄特异性病理变化。当给9至12日龄的小鼠进行一系列L-BSO注射时，会形成致密性白内障，尽管存活率很高且没有其他明显的长期影响。相比之下，对14至17日龄的小鼠进行类似处理，虽然在降低谷胱甘肽水平方面效果稍差，但经常导致死亡、后腿麻痹或精子发生受损，但不会产生白内障。给断奶前小鼠施用L-BSO为通过耗尽晶状体谷胱甘肽诱导白内障提供了一种新的模型系统，并可能有助于研究谷胱甘肽在出生后早期发育过程中晶状体和其他生长组织中的关键功能。
