It is known that Long-Evans Cinnamon (LEC) rats are characterized by the fulminant hepatitis occurring as a result of an abnormal hepatic deposition of Cu due to the lack of the Cu-transporter p-type ATPase. To prevent the hepatitis, two Zn compounds, Zn acetate and polaprezinc were given orally to LEC rats aged 30 days. At 100 days after birth, the control group composed of LEC rats fed a basal diet (Cu, 17 ppm; Zn, 50 ppm; Fe, 150 ppm) exhibited slight jaundice and showed high activities of serum enzymes related to hepatic function. The groups fed the diet fortified (1000 ppm as Zn) with Zn acetate or polaprezinc did not have jaundice. The hepatic Cu concentrations were 174 +/- 34 micrograms/g and 156 +/- 23 micrograms/g in the polaplezinc group and Zn acetate group, respectively. The control group showed 267 +/- 17 micrograms Cu/g and 298 +/- 62 micrograms Fe/g in the liver. The Fe concentration was about 1.7 times the concentration in the two Zn groups. Hepatic free Cu and Fe concentrations were 2.6 +/- 0.3 and 21.4 +/- 5.8 micrograms/g, 1.7 +/- 0.7 and 6.8 +/- 1.1 micrograms/g, and 1.3 +/- 0.1 and 6.2 +/- 0.8 micrograms/g in the control, polaprezinc and zinc acetate groups, respectively. Intestinal metallothionein (MT) concentrations were not increased significantly by the Zn diets. The two Zn compounds inhibit Cu absorption from the intestinal tract, resulting in a decrease of hepatic Cu deposition. The new Zn compound as well as Zn acetate is categorized as a therapeutic drug for Cu poisoning, including Wilson's disease.