Abstract
Twelve Holstein steers in a completely randomized block design were fed either a basal diet (concentrate:silage or hay at a DM ratio of 35:65) plus Cu sulfate at 20ppm of Cu (Cu-supplemented diet) or a basal diet plus ammonium molybdate to obtain 10ppm of Mo (Cu-depleting diet) on a DM basis in the whole diet for 8 mo. Supplemental Mo was utilized in the Cu-depleting diet to develop a Cu-deficient group. Molybdenum slowly accumulated in the liver in the group fed the Cu-depleting diet. Copper concentrations in the liver and polymorphonuclear neutrophils decreased in the Cu-deficient group compared with the Cu-sufficient group. Plasma Cu concentration did not change during the trial for the Cu-sufficient group. In the Cu-deficient group, plasma Cu concentrations increased during the first 3 mo of the trial, then declined, and remained unchanged for the last 5 mo. Superoxide dismutase activities in red blood cells, polymorphonuclear neutrophils, and whole blood decreased in the Cu-deficient group. Phagocytic capacity was not affected by Cu status, but killing capacity was decreased by low Cu status in the Cu-deficient group by the end of the trial. Glutathione peroxidase activity was unaffected by Cu status. Clinical symptoms of Cu-deficiency were not observed in this trial; there was no evidence of blood hemoglobin or BW gain difference between the two groups. In this study, Cu status affected its distribution in the tissues and related enzyme activities as well as bactericidal function of neutrophils.
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