Male Malin x Polled Dorset crossbred sheep were stall-fed with grass (10%) and PKC (90%) and supplemented with either zinc at 500 ug/g, as zinc sulfate (PKC+Zn group) or zinc (113 ug/g) and ammonium molybdate (500 ug/g) (PKC+Zn+Mo group) or unsupplemented diet (PKC group) for 20 weeks. Another group which acts as a control was fed with a diet consisting of corn and fish meal (2 0%) and grass (80%). The animals were monitored daily and the body weights were recorded at a period of two weeks intervals throughout the trial. Blood samples were also collected for mineral analysis. At the end of the trial the animals were slaughtered. The carcasses were examined for gross lesions, whilst the right liver lobes and renal cortex were isolated for histopathological evaluation and mineral analysis. All animals in the PKC group died before the end of the trial with the main clinical signs of generalised jaundice and haemoglobinuria. The kidneys were firm, enlarged and reddened or darkened. Histologically, the hepatocytes were swollen, vacuolated and necrotized, particularly at the periacinar zone. Hepatic fibrosis was observed at the periportal zone. Cellular swelling, vacuolation and necrosis were found in the tubular epithelial cells of the renal cortex. Neither clinical signs nor gross or remarkable histological lesions were observed in the other groups of animals. The hepatic, renal and blood copper levels In the PKC group were elevated when compared to the control. Addition of zinc either with or without ammonium molybdate in PKC diet inhibit the copper content in the organs, however the zinc contents were increased. The average daily gain of the PKC group was remained consistent to those of the other groups, except it was reduced starting at about 1 to 2 weeks prior to death. It was concluded that feeding PKC In excess in sheep can cause chronic copper toxicity. However, this effect can be prevented by dietary zinc supplementation either with or without ammonium molybdate.