Thirty-six yearling Hereford heifers were randomly allotted to one of the following treatments for a 120-day trial period: (1) no molybdenum, no copper; (2) no molybdenum, 1 g copper sulfate daily in cottonseed meal; (3) no molybdenum, single initial injection of 2 ml copper glycinate (120 mg copper); (4) 100 ppm molybdenum in the ration, no copper; (5) 100 ppm molybdenum, 1 g copper sulfate; (6) 100 ppm molybdenum, 2 ml copper glycinate injection.
All animals received grass hay ad libitum plus 500 g cottonseed meal daily. This ration contained 4.5 ppm copper and 2.5 ppm molybdenum. Copper treatments had no effect on weight gains or feed consumption in the absence of molybdenum. Heifers receiving only molybdenum lost weight over 120 days, while those also receiving copper sulfate equaled the non molybdenum fed animals; however, those injected with copper glycinate were intermediate. Feed consumption followed a similar trend.
Added copper eliminated much of the toxic effect of molybdenum, but copper sulfate was more effective under the 120-day trial conditions. Plasma molybdenum was increased by added dietary molybdenum while plasma copper was raised by both additional copper treatments and added molybdenum. Copper glycinate increased the plasma copper and molybdenum levels more rapidly than copper sulfate, but was less influential at the end of the 120-day period. Liver molybdenum was increased by added molybdenum but was reduced by copper sulfate alone. Both copper sources raised liver copper levels initially, but the effect of copper glycinate was nonsignificant at 120 days. The increase in plasma copper when molybdenum was added to the diet and the lack of a similar increase in liver copper, suggests that a copper-molybdenum complex exists in the blood. The significant interaction between molybdenum and copper source on liver copper suggests part of this complexing occurs in the digestive tract and thus limits copper absorption.
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