Thiomolybdate – The Major Factor on Clinical Copper Deficiency

The availability of copper to ruminant animals is greatly influenced by the molybdenum, sulphur; and iron content of diets. It has long been known that molybdenum is involved in Cu deficiency (Phillipo et al, 1987; Bremner et al, 1987; Hurley and Doane, 1989; Moeini et al.1997). The purpose of this study was to examine the effects of a low copper diet (less than 1.6 mg/kg DM) and also with additional molybdenum, iron and sulphur on the copper status in two breeds of sheep.

Four 1 year -old Suffolk cross Mule white sheep (live weight 34 – 43 Kg) and Four 7 to 9 months old Scottish black Hebridean castrate sheep were fed a low copper diet in a pelleted form over 17 weeks period. This diet was a modification of that described by Mills et al (1976) with oat husk replacing cellulose. This basal diet had a mean copper content of less than 1.6 mg Cu/kg DM. In order to increase the molybdenum, sulphur and iron of the diet, molybdenum was added as ammonium molybdate (NH₄)₆ MO₇ O₂₄.4H₂O), while sulphur and iron were added as (NH₄)₂ SO4 AND FeSO₄. 7H₂O 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 (5 mg/kg DM), iron (600 mg/kgDM) and sulphur (3 g/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.

It can be concluded that the specific effect of molybdenum in producing clinical copper deficiency symptoms can be detected when molybdenum combined whit sulphur and passes through into blood which can deactivated Cu enzymes and the clinical signs are likely to be from thiomolybdate (MoS4) in the body. The only way to stop thiomolybdate toxicity through CuMoS4 complex formation is to provide a more available form of copper supplement.