Early biochemical and histological changes in rats exposed to a single injection of thioacetamide.

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.

Selenium status in patients with liver cirrhosis and alcoholism.

1. Selenium status and blood levels of other nutrients related to lipid peroxidation were studied in patients with advanced alcoholic liver cirrhosis, in male alcoholics who had been abstinent for at least 1 month and in healthy control subjects. 2. Plasma Se was decreased in alcoholic cirrhosis but not among alcoholics in abstinence. Platelet glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity was decreased in cirrhotic patients, whereas GSH-Px in blood and plasma was the same as in controls for both groups of patients. 3. Plasma retinol and plasma alpha-tocopherol were decreased in alcoholic cirrhosis, whereas plasma ascorbic acid was the same in all groups. 4. The decreases in platelet GSH-Px, plasma Se and alpha-tocopherol indicate a deranged antioxidant defence in patients with advanced alcoholic cirrhosis, but the levels of these and other nutrients were generally not correlated to common clinical chemical indicators of liver disease.