Clinical copper deficiency is the second most common mineral deficiency in the world, the main cause being high dietary levels of molybdenum, sulphur and iron. Phillippo et al, (1987) reported that clinical signs of deficiency resulted from high dietary Mo and S. However, Fe and S resulted in hypocupraemia but did not induce clinical signs of deficiency. Therefore is was concluded that clinical copper deficiency was due to a direct effect of dietary Mo and S on copper metabolism in ruminants. Mackenzie et al. (1997) reported that plasma copper levels were not an accurate indicator of copper status and unlikely to predict animals requiring copper supplementation. Caeruloplasmin is large copper enzyme and accounts for 88% of plasma copper and Mackenzie et al. (1997) proposed that a caeruloplasmin to plasma copper ratio may provide a more accurate biochemical indicator of copper status. This trial was designed to investigate the effect of dietary Mo, S and Fe on the copper status of the lambs.