Growth, reproduction and copper metabolism in animals exposed to elevated dietary levels of cadmium and zinc

• Main Author: Campbell, James Keir
• Published: University of Aberdeen 1978
• Subjects: 636
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.450607

I. The effects of cadmium and zinc at dietary concentrations typical of those that can arise as a result of adventitious contamination of feedstuffs were investigated. II. Cadmium (1.5 - 18 mg/kg) in the diet of rats induced copper deficiency over a period of 9 weeks when the diet contained 2.6 mg Cu/kg but not when it contained 7.8 mg Cu/kg. III. The effect of cadmium on copper status of rats was due to reduced copper absorption. Cadmium supplementation induced no measurable change in hepatic copper metabolism in rats. IV. Zinc at a concentration of 300-1000 mg/kg diet induced copper deficiency , in rats receiving 2.6 mg Cu/kg diet. The first signs of deficiency (achromotrichia) were evident four weeks after introduction to a diet containing 1000 mg Zn/kg. V. The combined effects of zinc and cadmium on copper status in rats were greater than the effect of zinc or cadmium alone. Zinc supplement ation did not protect rats against the effects of cadmium on copper metabolism. VI. Cadmium and zinc, separately and in combination reduced cortical bone thickness in the femur of rats. VII. Cadmium at a concentration of 3 mg/kg had no detectable effect on pregnant ewes maintained for the last 100 days of pregnancy on a semi-synthetic diet containing 2.5 mg Cu/kg. VIII. Zinc at a concentration of 150 mg/kg in the diet of pregnant ewes had no detectable adverse effects on the health of the sheep. At a concentration of 750 rag/kg diet zinc induced severe copper deficiency in pregnant ewes when the diet contained 2.5 mg Cu/kg. This level of zinc supplementation greatly reduced the viability of perinatal lambs. Increasing the copper content of the diet of ewes receiving 750 mg Zn/kg, from 2.5 to 10 mg/kg prevented the development of copper deficiency in the ewes but did not increase the viability of the lambs. IX. Cadmium (3m g/kg) in the diet of weanling lambs markedly reduced growth rate when the diet contained 2.5 or 4.5 ag Cu/kg. This effect of cadmium was partially alleviated by a dietary zinc concentration of 150 mg/kg. Low growth rate in the cadmium supplemented lambs was not a result of cadmium-induced copper deficiency although an increase in dietary copper concentration from 4.5 to 15 mg/kg stimulated growth rate. Cadmium reduced the activity of cytochome oxidase in the duodenal mucosa and this may have been responsible for the very low growth rate of these animals. Over a period of approximately 10 months cadmium (3 mg/kg diet) reduced the thickness of cortical bone in lambs. Over this period, the cadmium concentration of liver and kidney rose to a level at which they would probably be considered unfit for human consumption. X. Contrary to the findings of other workers, zinc at a concentration of 150 mg/kg diet induced rapid accumulation of copper in liver when the copper concentration in the diet of lambs was raised from 4.5 tolS.O mg/kg. This level of zinc was associated with an increase in the proportion of soluble hepatic copper bound to a protein fraction similar to metallothionein. The proportion of soluble hepatic copper located in this fraction was greatest when the diet was supplemented J with both zinc and cadmium. The accumulation of copper in sheep receiving 150 mg Zn/kg diet was indicative of derranged copper metabolism as copper accumulation was associated with increased hepatic iron concentration and reduced hepatic cytochrome oxidase activity. In calves maintained on a diet containing an adequate concentration of copper (12.5 mg/kg), cadmium at concentrations of 2.0 and 4;0 mg/kg prevented hepatic copper accumulation. When the copper concentration of the diet was reduced from 12.5 to 8 mg/kg, cadmium reduced the efficiency of feed utilization, induced iron accumulation in duodenal mucosa and liver, and caused changes in bone conformation similar to those observed in copper deficiency. Significant changes in liver copper concentration were not observed, however.