Dashti H, Jeppsson B, Hägerstrand I, Hultberg B, Srinivas U, Abdulla M, Joelsson B, Bengmark S
Pharmacol Toxicol. 1987 Mar;60(3):171-4. doi: 10.1111/j.1600-0773.1987.tb01727.x.
Liver injury was induced by one subcutaneous administration of thioacetamide (200 mg/kg b.wt.) and studied 24 and 48 hrs later. Levels of aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) increased after 24 and 48 hrs. The lysosomal enzymes beta-hexosaminidase (beta-NAG) and beta-glucuronidase (beta-GLU) increased significantly after 24 hrs, while the level of beta-GLU returned to normal after 48 hrs, but the activity of beta-NAG remained significantly high even after 48 hrs. Histopathological examination showed necrotic hepatocytes around the central vein with infiltration of macrophages, neutrophils and eosinophils. The plasma zinc level decreased after 24 hrs and returned to normal after 48 hrs. Liver zinc content increased simultaneously at 24 hrs, returning to normal after 48 hrs. No alterations of plasma copper were observed after 24 and 48 hrs. Copper content of the liver increased significantly after 24 and 48 hrs. The present study thus shows that one dose of thioacetamide results in profound liver injury and supplementation of zinc prior to and simultaneously with thioacetamide normalized plasma zinc, increased liver zinc content and reduced the increase of beta-NAG, but did not influence the histological changes.
通过皮下注射一次硫代乙酰胺（200毫克/千克体重）诱导肝损伤，并在24小时和48小时后进行研究。24小时和48小时后，天冬氨酸转氨酶（ASAT）和丙氨酸转氨酶（ALAT）水平升高。溶酶体酶β-己糖胺酶（β-NAG）和β-葡萄糖醛酸酶（β-GLU）在24小时后显著升高，而β-GLU水平在48小时后恢复正常，但即使在48小时后β-NAG的活性仍显著升高。组织病理学检查显示中央静脉周围有坏死的肝细胞，伴有巨噬细胞、中性粒细胞和嗜酸性粒细胞浸润。血浆锌水平在24小时后下降，48小时后恢复正常。肝脏锌含量在24小时时同时增加，48小时后恢复正常。在24小时和48小时后未观察到血浆铜的变化。肝脏铜含量在24小时和48小时后显著增加。因此，本研究表明，一剂硫代乙酰胺会导致严重的肝损伤，在硫代乙酰胺之前和同时补充锌可使血浆锌正常化，增加肝脏锌含量并减少β-NAG的升高，但不影响组织学变化。
