Kinoshita J H, Fukushi S, Kador P, Merola L O
Metabolism. 1979 Apr;28(4 Suppl 1):462-9. doi: 10.1016/0026-0495(79)90057-x.
Aldose reductase (AR) appears to initiate the cataractous process in galactosemic and diabetic animals. Sugars in excess are converted to polyols by lens AR. In sugar cataracts, polyols accumulate to levels substantial enough to cause a hypertonicity leading to lens fiber swelling. All other changes appear secondary to polyol accumulation and lens swelling. The development of sugar cataracts can be duplicated in organ culture. In culture, the various changes that occur were minimized or did not occur when inhibitors of AR were included in the medium. Moreover, AR inhibitors were shown to effectively delay the onset of sugar cataract development in animals. A defect in the corneal epithelium of diabetics became apparent in vitrectomy. One manifestation of this problem was the delay in the reepithelialization of denuded corneas. In examining this problem experimentally, the epithelium was removed from the corneas of diabetic and normal rats. The regeneration of epithelium in corneas of diabetic rats required a longer period than in the normal. The possibility that AR, active in the epithelium, was involved in this phenomenon was investigated. The corneal epithelium was removed from both eyes of a diabetic rat. One eye was treated topically with the AR inhibitor CP-45,634 while the other served as control. The eye treated with CP-45,635 regenerated epithelium much more quickly than the untreated eye. Other AR inhibitors had similar beneficial effects.
醛糖还原酶（AR）似乎在半乳糖血症和糖尿病动物中引发白内障形成过程。过量的糖被晶状体AR转化为多元醇。在糖性白内障中，多元醇积累到足以导致高渗的水平，从而导致晶状体纤维肿胀。所有其他变化似乎都是多元醇积累和晶状体肿胀的继发结果。糖性白内障的发展可以在器官培养中重现。在培养中，当培养基中加入AR抑制剂时，发生的各种变化被最小化或未发生。此外，AR抑制剂被证明能有效延迟动物糖性白内障发展的起始。糖尿病患者角膜上皮的缺陷在玻璃体切除术中变得明显。这个问题的一个表现是裸露角膜的再上皮化延迟。在通过实验研究这个问题时，从糖尿病大鼠和正常大鼠的角膜上移除上皮。糖尿病大鼠角膜上皮的再生比正常大鼠需要更长的时间。研究了在上皮中具有活性的AR参与这一现象的可能性。从一只糖尿病大鼠的双眼移除角膜上皮。一只眼睛局部用AR抑制剂CP - 45,634治疗，而另一只作为对照。用CP - 45,635治疗的眼睛上皮再生比未治疗的眼睛快得多。其他AR抑制剂也有类似的有益效果。
