Biochemical and substructural studies on hepatic and serum lipoprotein metabolism after acute liver injury induced by thioacetamide in rats

Abstract

The effect of an acute liver injury induced by thioacetamide (TAA) on hepatic and serum lipoprotein metabolism in rats was studied using biochemical and ultrastructural methods. A single dose of 100 mg TAA/kg body weight caused within 48 h a decrease of hepatic triglyceride (TG) output into the serum by about 50% in comparison to the controls. The steady state of serum TG concentration from 24 to 96 h after TAA treatment implies that the clearance of TG from serum must be diminished to the same extent as the hepatic TG output was found to decrease. Moreover, the TAA treatment caused changes in the electrophoretic mobility as well as in the concentration and composition of circulating serum-lipoproteins. The electrophoresis revealed a decrease in the alpha-band, which can be explained by the decrease in the high density lipoproteins (HDL) total lipid concentration. The pre-beta-migrating band disappeared, whereas a broad beta-mobility band appeared, which most likely consists of a mixture of very low density lipoproteins (VLDL) and low density lipoproteins (LDL) as can be concluded from the changes in concentration and composition of lipids in both fractions. For a better visualization of the VLDL-forming capability in perilobular and centrolobular liver parenchymal cells of the TAA-treated animals the VLDL secretion blocking agent colchicine was used. It was shown that in comparison with colchicine-treated controls the VLDL secretory products are accumulated at a considerably lower rate manifested in a diminution of VLDL clusters, secretory vesicle size and the number of intravesicular VLDL particles.(ABSTRACT TRUNCATED AT 250 WORDS)