Beyer-Mears A, Cruz E
Diabetes. 1985 Jan;34(1):15-21. doi: 10.2337/diab.34.1.15.
Aldose reductase is implicated in the pathogenesis of diabetic cataracts; therefore, inhibition of this enzyme subsequent to cataractogenesis may represent a therapeutic approach for restoration of lens physiology. In the present study, the effect of aldose reductase inhibition subsequent to stage I cataract formation was investigated in the streptozocin-induced diabetic rat. Our results indicated that the aldose reductase inhibitor sorbinil, a spirohydantoin, arrested further progression and promoted a reparative process despite continuation of hyperglycemia and elevated lens glucose. Quantitative analysis of scanning electron micrographs indicated that the afflicted lens regions were contained and their cellular components stabilized with regard to fiber hydration and interdigitation. The reparative process included: normalization of lens sorbitol, gradual recovery of existing fiber contour and interdigitation, production of new fibers, and partial restoration of lens myo-inositol content.
醛糖还原酶与糖尿病性白内障的发病机制有关；因此，在白内障形成后抑制该酶可能是恢复晶状体生理功能的一种治疗方法。在本研究中，我们在链脲佐菌素诱导的糖尿病大鼠中研究了I期白内障形成后醛糖还原酶抑制的作用。我们的结果表明，醛糖还原酶抑制剂索比尼尔（一种螺乙内酰脲）尽管血糖持续升高且晶状体葡萄糖水平升高，但仍能阻止进一步发展并促进修复过程。扫描电子显微镜照片的定量分析表明，患病的晶状体区域得到控制，其细胞成分在纤维水合和交叉指状化方面趋于稳定。修复过程包括：晶状体山梨醇正常化、现有纤维轮廓和交叉指状化逐渐恢复、新纤维产生以及晶状体肌醇含量部分恢复。
