実験的糖尿病ラットにおける水晶体, 房水, 硝子体の生化学的変化とアルドース還元酵素阻害剤TATの影響

抄録

The etiology of diabetic cataract is usually explained by the following process; the conversion of glucose and galactose to polyol by aldose reductase, then the accumulation of polyol in lens, and the opacity of lens. Another explanation is that the hyperoxidation of lens membrane due to an increase of active oxigen and lipid peroxide in lens induces diabetic cataract. The experimental animals used in the present study were rats with galactose cataract and streptozotocin cataract. We measured the levels of antioxidants (glutathione, ascorbic acid) and lipid peroxide (malonodialdehyde) in lens, aqueous humor and vitreous body. Furthermore we studied the effects of aldose reductase inhibitor (TAT) on these levels. In streptozotocin diabetes rats, the increased malonodialdehyde levels in lens, aqueous humor and serum were suppressed by TAT administration. In galactose and streptozotocin diabetes rats, the decreased levels of glutathione and ascorbic acid were suppressed by TAT administration.