In female Wistar rats the animal model of TAA-induced liver cirrhosis has been tested for reliability and usefulness for studies on lipid and lipoprotein metabolism in cirrhosis. From our results we draw the following conclusions: Application of 300 mg TAA/l drinking water from the 4th to the 6th month of life leads in all treated rats to liver cirrhosis which is rather uniformly of micronodular surface morphology. Under this treatment the survival rate is about 90 percent. Increasing the administered dose (450 and 600 mg/l) and/or extension of TAA administration time (4 or more months) leads to decreasing survival rates, and to a shift from micronodular towards macronodular cirrhosis. To produce macronodular cirrhosis it is suggested to extent the application time rather than to increase the dose since in the latter case the survival rate is very low. The alterations of lipid and lipoprotein metabolism observed in this animal model, i.e. decrease of pre-beta-lipoproteins, increase of beta-lipoproteins, decrease of serum triglyceride concentration and decrease of hepatic VLDL-TG output into the serum are in good agreement with those observed in human cirrhosis. Thus, the TAA-induced chronic liver injury proved to be a reliable and useful model for studies on lipid and lipoprotein metabolism in liver cirrhosis.