NEAR-TOTAL GLUTATHIONE DEPLETION AND AGE-SPECIFIC CATARACTS INDUCED BY BUTHIONINE SULFOXIMINE IN MICE
NEAR-TOTAL GLUTATHIONE DEPLETION AND AGE-SPECIFIC CATARACTS INDUCED BY BUTHIONINE SULFOXIMINE IN MICE
复制标题
DOI：
10.1126/science.3726547
复制
发表时间：
1986-08-01
期刊：
影响因子：
56.9
通讯作者：
WORGUL, BV
中科院分区：
文献类型：
--
作者：
CALVIN, HI;MEDVEDOVSKY, C;WORGUL, BV
谷胱甘肽生物合成的特异性抑制剂L-丁硫氨酸亚磺胺(L-BSO)虽然对成年小鼠相对无毒，但重复给药会导致雄性哺乳小鼠严重的谷胱甘肽耗竭和特定年龄的病理变化。尽管存活率很高，而且没有其他显著的长期影响，但在给9至12天的小鼠注射一系列L-BSO后，小鼠仍出现了密集的白内障。相比之下，对14至17天的小鼠进行类似的治疗，尽管在降低谷胱甘肽水平方面效果略差，但经常会导致死亡、后腿瘫痪或精子生成障碍，但不会产生白内障。给予早期断奶小鼠L-BSO为晶状体谷胱甘肽耗竭诱发白内障提供了一种新的模型系统，并可能为研究谷胱甘肽在晶状体和其他生长组织中的关键功能提供了可能。
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.