Thiomolybdate – The Major Factor on Clinical Copper Deficiency

Abstract

respectively. Feed samples were analysed for minerals Mo, Fe, S and Cu content by Inductive coupled plasma (ICP). Changes in liver and blood copper concentration and in the copper-containing enzymes; caeruloplasmin (CP) and superoxide dismutase (SOD) activities were monitored by standard methods described by Mackenzie et al, (1997). Statistical analysis of the results was carried out using student T test and analysis of variance (one way). The results showed that the occurrence of Cu deficiency depends not only on the low content of this metal in an animals diet, but also on the presence of interacting other minerals, especially molybdenum, sulphur and iron. Although the blood copper and liver copper concentration decreased in all sheep fed a low copper diet no clinical signs of deficiency were observed over 17 week period. The response of the animals to the dietary alteration depends on the liver copper concentration and breed. The black Hebridean Sheep were more susceptible than Suffolk sheep showing clinical copper deficiency. The mean overall balance results for the black and white sheep were -0.063 and +0.013 mg Cu/day respectively over this 17 weeks depletion period. The values of total plasma copper and TCA soluble copper plasma and copper related enzymes (SOD, CP) are shown in figures. The plasma copper levels for the white sheep during the initial depletion period ranged from 10.8 to 17.8 µmol/ and for the black sheep were lower with the range being 6 - 14 mmol/l. There were no significant differences between the copper plasma and TCA soluble copper plasma during this phase of the experiment. However the addition of molybdenum (5mg / kg DM), iron (600mg/kgDM) and sulphur (3g /kg dm) to this diet after 2-5 weeks did produce clinical copper deficiency with dipigmentation of wool and poorer crimp being observed. In third phase of the experiment when the diet was further modified by the removal of the molybdenum but still with 600 mg/kg DM iron and 3-g/kg DM sulphur, there was a decrease in blood copper but no clinical symptoms were observed. This is in agreement with Humphries et al. (1983), Bremner et al. (1987) and SUTTLE (1991) who showed that iron can act as a potent antagonist of copper and can also severely reduce the concentrations of copper without producing clinical symptoms of copper deficiency.