3β-(2-二乙氨基乙氧基)-雄甾-5-烯-17-酮盐酸盐（U18666A）诱导大鼠白内障形成过程中的胆固醇与脂质过氧化作用。
Cholesterol and lipid peroxidation in 3 beta-(2-diethylaminoethoxy)- androst-5-en-17-oneHCl (U18666A) induced cataractogenesis in rats.
作者信息
Yadav S, Rawal U M
机构信息
Department of Zoology, School of Sciences, Gujarat University, Ahmedabad, India.
出版信息
Indian J Exp Biol. 1992 Feb;30(2):147-8.
Decrease in cholesterol was observed in precataractous, cataractous, advance nuclear cataractous and non-cataractous lenses when 3 beta-(2-diethylaminoethoxy)-androst-5-en-17- oneHCl (U18666A) was injected, sc, to rats. Significant increase in lipid peroxidation was observed before the onset of any apparent lenticular opacity in U18666A treated rats. The results suggest that decrease in cholesterol is capable of altering the structural integrity of lens fibers. However, 12.5% decrease in cholesterol and 5% increase in lipid peroxidation observed in non-cataractous lenses indicated that these changes are not sufficient for any apparent opacification.
当向大鼠皮下注射3β-(2-二乙氨基乙氧基)-雄甾-5-烯-17-酮盐酸盐（U18666A）时，在白内障前期、白内障期、晚期核性白内障期和非白内障晶状体中均观察到胆固醇降低。在接受U18666A治疗的大鼠中，在任何明显的晶状体混浊出现之前，均观察到脂质过氧化显著增加。结果表明，胆固醇降低能够改变晶状体纤维的结构完整性。然而，在非白内障晶状体中观察到胆固醇降低12.5%以及脂质过氧化增加5%，这表明这些变化不足以导致任何明显的混浊。
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