Weber W, Kehrer T, Gressner A M, Stuhlsatz H W, Greiling H
J Clin Chem Clin Biochem. 1983 May;21(5):287-93. doi: 10.1515/cclm.1983.21.5.287.
The catalytic activities of 4 glycosidases (hyaluronate-4-glycanohydrolase (EC 3.2.1.35), beta-N-acetyl-D-glucosaminidase (EC 3.2.1.30), beta-glucuronidase (EC 3.2.1.31), alpha-L-iduronidase (EC 3.2.1.76)), of the arylsulphatases A and B (EC 3.1.6.1) and of the protease cathepsin D (EC 3.4.23.5) were measured in extracts from hepatocytes and non-parenchymal cells and in serum during the development of thioacetamide-induced rat liver fibrosis (22 weeks). In non-parenchymal liver cells the catalytic activities of beta-N-acetyl-D-glucosaminidase, beta-glucuronidase, alpha-L-iduronidase and cathepsin D were increased significantly during chronic liver damage, but that of hyaluronate-4-glycanohydrolase was reduced by 40 to 65% during the period of application of thioacetamide. The catalytic activities of the arylsulphatases were lowered by 65% compared to control values in the 12th week but with advancing liver damage the catalytic activities returned to nearly normal values. Parenchymal cells of rats, which had been liver-damaged for 6 months, contained strongly elevated activities of beta-glucuronidase, beta-N-acetyl-D-glucosaminidase, arylsulphatases A and B, and cathepsin D but only slightly increased activities of hyaluronate-4-glycanohydrolase and alpha-L-iduronidase, respectively. In the serum of liver-damaged rats the activity of alpha-L-iduronidase was strongly elevated, while that of N-acetyl-beta-D-glucosaminidase was only slightly increased. The activities of beta-glucuronidase and of arylsulphatases A and B were decreased during the whole period of treatment. The catalytic functions of hyaluronate-4-glycanohydrolase and of cathepsin D, respectively, were decreased initially, but both enzyme activities were elevated during the more advanced stages of long term thioacetamide treatment.
在硫代乙酰胺诱导的大鼠肝纤维化(22周)发展过程中,测定了肝细胞和非实质细胞提取物以及血清中4种糖苷酶(透明质酸-4-聚糖水解酶(EC 3.2.1.35)、β-N-乙酰-D-葡萄糖胺酶(EC 3.2.1.30)、β-葡萄糖醛酸酶(EC 3.2.1.31)、α-L-艾杜糖醛酸酶(EC 3.2.1.76))、芳基硫酸酯酶A和B(EC 3.1.6.1)以及蛋白酶组织蛋白酶D(EC 3.4.23.5)的催化活性。在非实质肝细胞中,β-N-乙酰-D-葡萄糖胺酶、β-葡萄糖醛酸酶、α-L-艾杜糖醛酸酶和组织蛋白酶D的催化活性在慢性肝损伤期间显著增加,但在硫代乙酰胺应用期间,透明质酸-4-聚糖水解酶的活性降低了40%至65%。与对照组相比,芳基硫酸酯酶的催化活性在第12周降低了65%,但随着肝损伤的进展,催化活性恢复到接近正常水平。肝损伤6个月的大鼠实质细胞中,β-葡萄糖醛酸酶、β-N-乙酰-D-葡萄糖胺酶、芳基硫酸酯酶A和B以及组织蛋白酶D的活性显著升高,但透明质酸-4-聚糖水解酶和α-L-艾杜糖醛酸酶的活性仅略有增加。在肝损伤大鼠的血清中,α-L-艾杜糖醛酸酶的活性显著升高,而N-乙酰-β-D-葡萄糖胺酶的活性仅略有增加。在整个治疗期间,β-葡萄糖醛酸酶以及芳基硫酸酯酶A和B的活性降低。透明质酸-4-聚糖水解酶和组织蛋白酶D的催化功能最初降低,但在长期硫代乙酰胺治疗的更晚期阶段,两种酶的活性均升高。