Abstract
An investigation has been in order to elucidate the mechanism of the elevation of serum enzyme activities and about the changes in subcellular distribution during development of experimentally produced hepatic damage in the rats. Two enzymes have been studied : acid phosphatase (Acid Pase) and N-acetyl-β-glucosaminidase (NAG). Three different methods of inducing hepatic damage have been used : administration of carbon tetrachloride (CCl4), dimethylnitrosamine (DMNA), and thioacetamide (TAA). In acute hepatic damage, an increase in soluble activity was found to occur for two enzymes studied. The extent of this increase was slightly much in the activity of NAG as compared with that of Acid Pase. The changes in serum NAG activity was remarkably much in the case of any drugs. During the development stages of chronic administration of CCl4, the subceliular distribution pattern of lysosomal enzymes after 4 weeks were similar to that of lysosomal enzymes after 12 weeks. At 4 weeks after the administration of CCl4, the changes of lysosomal enzymes activities in the plasma was similar to that of acute hepatic damage by the treatment with DMNA and TAA. Furthermore, in the plasma at 12 weeks after the administration of CCl4, the variation of lysosomal enzymes activities was clearly differed from that of acute hepatic damage. It is assumed that the changes in NAG activity is minor due to fibroblasts other than hepatic parenchymal cells for the origin of the increased serum NAG activity during the CCl4-chronic hepatic damage.
