Glycoprotein metabolism in dimethylnitrosamine induced hepatic fibrosis in rats

Glycoproteins play a major role in the pathogenesis of hepatic fibrosis by accumulating in the sinusoids and the space of Disse. In order to obtain more information about the altered metabolism of glycoproteins during the development of human hepatic fibrosis, the carbohydrate moieties of the glycoproteins were monitored in experimentally induced hepatic fibrosis. The liver injury was induced by injecting dimethylnitrosamine intraperitoneally in male albino rats. The injections were given on the first 3 consecutive days of each week over a period of 21 days. Glycoprotein moieties such as total hexose, hexosamine, fucose and sialic acid were estimated in liver, serum and urine samples on days 7, 14 and 21 of the experiment. The results indicated a significant decrease in total hexose and an increase in fucose levels in the liver tissue during dimethylnitrosamine administration. While protein bound hexose in the serum showed a significant decrease, sialic acid levels were notably increased. The other glycoprotein moieties both in liver and serum also showed an increase in the later periods of study, especially on day 21. All glycoprotein moieties exhibited a significant increase in the rate of urinary excretion on the 14th and 21st days, indicating an increased rate of metabolic degradation in the acute phase of hepatic fibrosis. The results suggest that glycoproteins undergo changes in both synthesis and the degradation during hepatic fibrosis. The relative alterations in these processes will play a vital role in determining the progression of hepatic fibrosis.