Stevens A
National Vision Research Institute of Australia, Carlton, Australia.
J Am Optom Assoc. 1995 Dec;66(12):744-9.
Recent data have favored non-enzymatic glycation as a likely mechanism in diabetic cataract formation. The advanced glycation end products (AGEs) that are formed lead to opacification of the lens by disrupting the short-range order between the proteins. Attempts to decrease AGE formation has led to the use of various anti-glycating agents. Their efficacy, however, has been questionable.
The extent of AGE formation was monitored in fetal bovine eyes using non-tryptophan fluorescence. The amount of carbohydrate bound to the proteins was measured after reduction with radio-labelled sodium borohydride.
While the addition of glucose, glucose-6-phosphate or fructose increased the levels of glycation by only 25 percent and the levels of AGEs by 40 percent, glyceraldehyde resulted in a 70 percent increase in glycation and showed extensive AGE formation (an increase of over 6600 percent when compared to the unglycated protein). The anti-glycating agents aspirin and ibuprofen were unable to significantly decrease the extent of bound metabolite or reduce the amount of AGE formed. In contrast, penicillamine and aminoguanidine were more effective in reducing the levels of AGEs, even though the levels of bound metabolite appeared unchanged.
Triose phosphates are likely to be the major metabolic intermediates that result in AGE formation. The anti-glycating agents, whereas penicillamine and aminoguanidine-which react with the Amadori-derived fragmentation products-significantly decreased levels of AGEs.
近期数据表明，非酶糖基化可能是糖尿病性白内障形成的机制。所形成的晚期糖基化终产物（AGEs）通过破坏蛋白质间的短程有序结构导致晶状体混浊。降低AGE形成的尝试促使人们使用各种抗糖基化剂。然而，它们的疗效一直存在疑问。
使用非色氨酸荧光监测胎牛眼内AGE的形成程度。用放射性标记的硼氢化钠还原后，测量与蛋白质结合的碳水化合物量。
虽然添加葡萄糖、6-磷酸葡萄糖或果糖仅使糖基化水平增加25%，AGE水平增加40%，但甘油醛使糖基化水平增加70%，并显示出大量AGE形成（与未糖基化蛋白质相比增加超过6600%）。抗糖基化剂阿司匹林和布洛芬不能显著降低结合代谢物的程度或减少AGE的形成量。相比之下，青霉胺和氨基胍在降低AGE水平方面更有效，尽管结合代谢物的水平似乎没有变化。
磷酸丙糖可能是导致AGE形成的主要代谢中间体。抗糖基化剂中，与阿马多利衍生的裂解产物反应的青霉胺和氨基胍显著降低了AGE水平。
