Unakar N J, Johnson M, Tsui J, Cherian M, Abraham E C
Department of Biological Sciences, Oakland University, Rochester, MI 48309-4401, USA.
Exp Eye Res. 1995 Aug;61(2):155-64. doi: 10.1016/s0014-4835(05)80035-1.
Germanium compounds have been shown to be effective in preventing the formation of advanced glycation end-products and for reversible solubilization of glycated proteins. As protein glycation has been proposed to play a role in lens opacification, we initiated studies to evaluate the effects of 2-carboxyethyl germanium sesquioxide (germanium compound 132 or Ge-132) on galactose-induced cataractogenesis. For this study young Sprague-Dawley rats were fed a 50% galactose diet. One group of rats received topical saline and another group was administered Ge-132 in saline four times a day. The lenses were periodically examined with an ophthalmoscope and at desired intervals processed for light and scanning electron microscopy. Our observations, beginning at 3 days and continuing to 21 days of galactose feeding, exhibited the characteristic galactose-induced morphological alterations, which include the formation of vacuoles, cysts, membrane disruption and swelling of fibers and epithelial cells as well as disorganization of the bow in lenses of rats in both groups. However, in the majority of rats administered Ge-132 these alterations were delayed as compared to the lenses of rats administered saline. Our findings show that, although the initiation, progression and pattern of lens opacification in rats receiving saline and Ge-132 were similar, in the majority of lenses the progression and establishment of mature cataracts in the Ge-132 group of rats were delayed. Analysis of the water-soluble and water-insoluble lens-protein fractions for glycated proteins showed increased levels of the Amadori products and advanced glycation related fluorescent products in galactosemic rats treated with saline eye drops. In rats receiving the topical Ge-132 treatment the levels of these glycation products were substantially reduced to levels lower than control values. Prevention of glycation seems to be a mechanism by which cataract progression is delayed.
锗化合物已被证明在预防晚期糖基化终产物的形成以及使糖化蛋白可逆溶解方面有效。由于蛋白质糖基化被认为在晶状体混浊中起作用，我们开展了研究以评估二氧化三羧乙基锗（锗化合物132或Ge - 132）对半乳糖诱导的白内障形成的影响。在本研究中，给年轻的斯普拉格 - 道利大鼠喂食50%的半乳糖饮食。一组大鼠接受局部生理盐水滴眼，另一组大鼠每天用生理盐水给予Ge - 132四次。定期用检眼镜检查晶状体，并在预定的时间间隔进行处理以用于光镜和扫描电子显微镜检查。我们从喂食半乳糖的第3天开始并持续到第21天的观察结果显示出半乳糖诱导的特征性形态学改变，这包括两组大鼠晶状体中出现空泡、囊肿、膜破坏、纤维和上皮细胞肿胀以及晶状体弓的紊乱。然而，与接受生理盐水滴眼的大鼠晶状体相比，在大多数给予Ge - 132的大鼠中这些改变出现延迟。我们的研究结果表明，尽管接受生理盐水和Ge - 132的大鼠晶状体混浊的起始、进展和模式相似，但在大多数晶状体中，Ge - 132组大鼠成熟白内障的进展和形成被延迟。对半乳糖血症大鼠晶状体蛋白的水溶性和水不溶性部分的糖化蛋白分析表明，用生理盐水滴眼治疗的大鼠中阿马多里产物和晚期糖基化相关荧光产物的水平升高。在接受局部Ge - 132治疗的大鼠中，这些糖基化产物的水平大幅降低至低于对照值的水平。预防糖基化似乎是延迟白内障进展的一种机制。
