Kirschbaum B B, Bosmann H B
J Med. 1975;6(1):97-111.
Diacetylbenzidine was used to induce a nephrotic syndrome in female rats. Enzymes involved in glycoprotein metabolism were evaluated during an early stage of induced renal disease before extensive histologic changes occurred. The results show that lysosomal acid hydrolases are not activated or released to any measurable degree during the early stages of the disease. Minimal differences in the composition of glomerular basement membrane of nephrotic rats were found despite heavy proteinuria. Glomerular specific activities of certain glycoprotein:glycosyl transferases were depressed in nephrotic animals. A new viewpoint to explain the pathology of glomerular proteinuria is presented based on the phenomenon of sublethal autolysis affecting cell surface structure and function, of which activity levels of glycoprotein:glycosyl transferases are an example. Increased activities of glycosyl transferases and Na-D ATPase were noted in the cortex from nephrotic animals. These studies involving cortex indicate that the pathologic process is not confined to the glomerulus and may contribute information concerning Na+ transport in the nephrotic rat.
用二乙酰联苯胺诱导雌性大鼠患肾病综合征。在诱导的肾脏疾病早期,即在广泛的组织学变化出现之前,对参与糖蛋白代谢的酶进行了评估。结果表明,在疾病早期,溶酶体酸性水解酶未被激活或释放到任何可测量的程度。尽管有大量蛋白尿,但肾病大鼠肾小球基底膜的组成差异极小。肾病动物中某些糖蛋白:糖基转移酶的肾小球比活性降低。基于影响细胞表面结构和功能的亚致死性自溶现象,提出了一种解释肾小球蛋白尿病理的新观点,糖蛋白:糖基转移酶的活性水平就是一个例子。在肾病动物的皮质中,糖基转移酶和钠 - D - ATP酶的活性增加。这些涉及皮质的研究表明,病理过程并不局限于肾小球,可能会提供有关肾病大鼠钠转运的信息。