Wormser U, Zbinden G
Arch Toxicol. 1986 Jul;59(2):111-4. doi: 10.1007/BF00286733.
Serum proteolytic activity was determined in galactosamine-treated rats and in controls. Injection of the hepatotoxin at a dose of 400 mg/kg resulted in a 3.4-fold elevation in the serum proteolytic activity, while AST (aspartate aminotransferase), ALT (alanine aminotransferase) and bilirubin were increased by factors of 3.9, 8.8 and 4.5, respectively. Studies with proteinase inhibitors revealed that the serum proteolytic activity was partially metal-dependent as well as puromycin and antipain sensitive. Differences in susceptibility to a combination of N-ethylmaleimide and antipain indicated presence of different proteolytic systems in the sera of liver damaged and control rats. Separation of serum proteinases by gel filtration showed that the galactosamine-intoxicated rat serum contained activity which did not appear in the control serum. This activity was partially metal dependent, antipain and N-ethylmaleimide sensitive, and was more susceptible to dithiothreitol than the control activity. These findings demonstrate that hepatocellular damage induced by galactosamine caused not only an increase in serum proteinases, but was also associated with the appearance of enzymes not normally released by the liver of untreated animals.
在经半乳糖胺处理的大鼠和对照组中测定了血清蛋白水解活性。以400mg/kg的剂量注射肝毒素导致血清蛋白水解活性升高3.4倍,而天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)和胆红素分别升高了3.9倍、8.8倍和4.5倍。蛋白酶抑制剂研究表明,血清蛋白水解活性部分依赖金属,对嘌呤霉素和抗痛素敏感。对N-乙基马来酰亚胺和抗痛素组合的敏感性差异表明,肝损伤大鼠和对照大鼠血清中存在不同的蛋白水解系统。通过凝胶过滤分离血清蛋白酶表明,半乳糖胺中毒大鼠血清中的活性在对照血清中未出现。该活性部分依赖金属,对抗痛素和N-乙基马来酰亚胺敏感,并且比对照活性对二硫苏糖醇更敏感。这些发现表明,半乳糖胺诱导的肝细胞损伤不仅导致血清蛋白酶增加,还与未处理动物肝脏中通常不释放的酶的出现有关。