Unakar N J, Tsui J, Johnson M
Department of Biological Sciences, Oakland University, Rochester, MI, USA.
Curr Eye Res. 1997 Aug;16(8):832-7. doi: 10.1076/ceyr.16.8.832.8980.
Recently, we reported that topical administration of 2-carboxyethyl germanium sesquioxide (Ge-132) concurrently with 50% galactose feeding delayed the establishment of mature cataracts and reduced advance glycation product. This study was to determine the effect of pretreatment of Ge-132 on galactose associated morphological changes and Na(+)-K(+)-ATPase activity.
Young Sprague Dawley rats received topical eye drops four times a day of either saline or Ge-132 seven days prior to the 50% galactose diet and during galactose feeding. At desired intervals the lenses were extracted, photographed and processed for either light microscopy, scanning electron microscopy or the determination of Na(+)-K(+)-ATPase activity.
In Ge-132 pretreated lenses as compared to saline pretreated lenses the following results were observed: (a) the galactose-induced morphological alterations in the majority of lenses were delayed and (b) Na(+)-K(+)-ATPase activity was protected.
Our previous and current studies show that in addition to osmotic stress post-translational protein modification, such as glycation, including enzymes may play a role in initiating changes that lead to cataract development. The inhibition of protein glycation by antiglycating compounds, such as Ge-132, delays sugar cataract formation. Currently, we are investigating the status of protein glycation and advanced glycation end products following pretreatment with Ge-132 and the role of Ge-132 on the activities of enzymes such as aldose reductase and Na(+)-K(+)-ATPase.
最近,我们报道了局部应用二氧化三羧乙基锗(Ge - 132)并同时喂食50%半乳糖可延缓成熟白内障的形成并减少晚期糖基化终产物。本研究旨在确定Ge - 132预处理对半乳糖相关形态学变化和钠钾ATP酶活性的影响。
年轻的斯普拉格 - 道利大鼠在给予50%半乳糖饮食前7天及喂食半乳糖期间,每天接受4次局部滴眼,滴注生理盐水或Ge - 132。在预定时间间隔取出晶状体,拍照并进行处理,用于光学显微镜检查、扫描电子显微镜检查或钠钾ATP酶活性测定。
与生理盐水预处理的晶状体相比,Ge - 132预处理的晶状体观察到以下结果:(a)大多数晶状体中半乳糖诱导的形态学改变延迟;(b)钠钾ATP酶活性得到保护。
我们之前和当前的研究表明,除了翻译后蛋白质修饰(如糖基化)引起的渗透应激外,包括酶在内可能在引发导致白内障发展的变化中起作用。抗糖基化化合物(如Ge - 132)对蛋白质糖基化的抑制作用可延缓糖性白内障的形成。目前,我们正在研究Ge - 132预处理后蛋白质糖基化和晚期糖基化终产物的状态,以及Ge - 132对醛糖还原酶和钠钾ATP酶等酶活性的作用。