No abstract

Thirty 6-yr-old Targhee ewes were randomly allotted to one of five supplemental treatments to evaluate supplementation effects on liver and fecal Zn and Cu concentrations and serum alkaline phosphatase activity: 1) control, 2) Zn complex, 3) Zn and Cu (ZnCu) complex, 4) Zn sulfate, and 5) ZnCu sulfates. Supplements were administered daily in gelatin capsules for 56 d. Liver biopsies and serum samples were collected every 14 d starting on d 0. Supplemental Zn and Cu levels were formulated to provide 90 mg/kg Zn and 10 mg/kg Cu, respectively, on a daily dry matter intake basis. Form (complex vs sulfate) x type (Zn vs ZnCu) interactions were not detected (P > 0.35). Therefore, contrast statements were used to make the following treatment comparisons: 1) control vs supplement, 2) Zn vs ZnCu, and 3) complex vs sulfate. Ewe BW at the end of the study (P = 0.09) and ewe BW change from beginning to end of the study (P = 0.07) were greater for supplemented than control ewes. Body weight and BW change did not differ between sulfate and complex (P > 0.39) or Zn- and ZnCu- (P > 0.40) supplemented ewes. Liver Cu concentrations did not differ (P = 0.41) between control and supplemented ewes. Liver Cu concentrations were higher (P < 0.10) for ewes supplemented with ZnCu than Zn and complex than sulfate forms of supplement. Liver Zn concentration tended (P = 0.13) to be higher in ZnCu than Zn-supplemented ewes. Liver and fecal Zn concentration were higher (P < 0.06) in ewes fed complex than sulfate supplements. However, serum alkaline phosphatase activity tended (P = 0.12) to be greater in ewes fed sulfate than complex supplements. Supplementing mature ewes with complexed minerals resulted in higher concentrations of Zn and Cu in the liver. In addition, supplemental Cu tended to increase concentrations of Zn in the livers of ewes; however, high levels of supplemental Zn did not negatively impact liver Cu concentrations.

The objective of this study was to evaluate the rate and extent of Cu repletion in Holstein heifers using two Cu sources (organic and inorganic) at two levels (15 and 30 mg/kg). An additional repletion treatment included a Cu oxide bolus. Heifers (n = 50) were individually fed a total mixed ration fortified with S and Mo at 0.40%, and 15 mg/kg of dry matter of the total diet, respectively. After 111 d of depletion, heifers were stratified by liver Cu concentration and randomly allotted to one of five repletion treatments. Four treatments consisted of feed sources of Cu (feed-Cu), 1) CuSO4 at 15 mg/kg; 2) CuSO4 at 30 mg/kg; 3) Availa-Cu at 15 mg/kg; and 4) Availa-Cu at 30 mg/kg. Availa-Cu is an organic Cu source that produces a Cu-amino acid complex. A fifth treatment, consisting of an intraruminal bolus (IB), provided a single dose of 25 g of CuO needles. Repletion treatments were delivered in the same total mixed ration without supplemental S and Mo. Copper status was assessed in blood and liver samples collected on 14-d intervals for 70 d. Irrespective of treatment, all heifers increased in body weight during the repletion period. Liver Cu increased in each feed-Cu treatment over time. Heifers treated with an IB reached a peak in liver Cu concentration (165.5 mg/kg) on d 28. Mean liver Cu concentrations were higher in heifers receiving 30 mg/kg of Cu compared with heifers receiving 15 mg/kg of Cu. Red blood cell superoxide dismutase (SOD) activity was higher (P < 0.001) in heifers receiving CuSO4 than Availa-Cu (0.98 vs 0.87 U). Also, SOD activity was higher when heifers were supplemented with 30 vs 15 mg/kg Cu (0.98 vs 0.87 U). Heifers receiving the Cu IB had higher SOD activity than heifers receiving feed-Cu sources (1.03 vs 0.92 U). Plasma ceruloplasmin concentration was higher (P < 0.001) in IB-treated heifers vs. other treatments. No differences in plasma ceruloplasmin were detected for feed-Cu source or level. These results indicate that all Cu sources evaluated in this study elevated Cu status of depleted heifers, particularly when provided at higher dietary levels.

Performance, immune response, and liver trace mineral status were measured in growing heifers supplemented with different copper (Cu) concentrations and sources when diets contained the Cu antagonists Mo, S, and Fe. Sixty Angus x Hereford heifers were managed in two groups for 112 d and were either individually fed diets and mineral treatments using individual feeding stalls (Stall) or pen-fed grass hay and individually supplemented mineral treatments (Pen). The basal diet of grass hay, rolled barley, and soybean meal was analyzed to contain 6 mg Cu/kg DM. The treatments consisted of 1) no supplemental Cu (Control); 2) 49 mg Cu/kg DM from Cu sulfate (i.e. approximately five times NRC recommendation for Cu from CuSO4) (5X-SO4); 3). 22 mg Cu/kg DM from CuSO4 (2X-SO4); 4). 22 mg Cu/kg DM from a combination of 50% CuSO4 and 50% Cu-amino acid complex (50-50); and 5). 22 mg Cu/kg DM from a combination of 25% CuSO4, 50% Cu-amino acid complex, and 25% Cu oxide (CuG) (25-50-25). All heifers were supplemented with the Cu antagonists Mo (10 mg/kg DM), S (2,900 mg/kg DM), and Fe (500 mg/kg DM). These diets resulted in dietary Cu:Mo ratios that averaged 0.5:1 for Control, 4.5:1 for the 5X-SO4, and 2.4:1 for 2X-SO4, 50-50, and 25-50-25. Rate and efficiencies of gain and cell-mediated immune function were not different (P > 0.10) among treatments. Data suggest supplements containing combinations of inorganic and complexed Cu interacted differently in the presence of Mo, S, and Fe. Heifers consuming the 25-50-25 supplement in the Stall group initially lost hepatic Cu rapidly but this loss slowed from d 50 to d 100 compared to the Control (P = 0.07), 50-50 (P < 0.05), and 2X-SO4 (P < 0.05) heifers and was similar (P > 0.10) to that in the 5X-SO4 heifers. In the Pen group, total hepatic Cu loss tended to be greater for 25-50-25 and 2X-SO4 compared to 5X-SO4 heifers (P = 0.09 and P = 0.06, respectively); Cu loss in the 50-50 heifers was similar (P > 0.10) to that in the 5X-SO4 heifers. This suggests that supplementing combinations of inorganic and amino acid-complexed Cu was as effective in limiting hepatic Cu loss during antagonism as was increasing dietary Cu levels to five times the NRC recommendation. A combination of 25% CuSO4 , 50% Cu-amino acid complex, and 25% CuO limited liver accumulation of Mo compared to supplements without CuO and could provide a strategic supplementation tool in limiting the systemic effects of Cu antagonism in beef cattle.

Yearling Targhee ewes (n = 24; not pregnant or lactating) were used in a 2 x 2 factorial arrangement of treatments to determine the effects of supplemental vitamin E (0 IU [0vitE] vs 330 IU vitamin E x ewe(-1) x d(-1) [+vitE]) and Zn (0 mg [0Zn] vs 140 mg Zn x ewe(-1) x d(-1) [+Zn]) on serum alpha-tocopherol concentrations, antibodies to parainfluenza type 3 (PI3), ewe BW, Zn liver concentrations, and serum alkaline phosphatase activity. Ewes were managed as one group, grazed native pasture, and had ad libitum access to white salt and water. Ewes that received supplemental vitamin E were orally dosed every other day with 660 IU of DL-alpha-tocopherol acetate in a gelatin capsule beginning on d 1 and continuing to d 63 of the study. Ewes that received Zn supplement were orally dosed every other day with 280 mg of Availa-Zn 100 (Zinpro Corp., Eden Prairie, MN, IFN 6-32-054) in gelatin capsules for 63 d. All ewes were vaccinated with killed PI3 on d 22 and 42. No interactions were detected (P > 0.35); however, serum alpha-tocopherol concentrations and PI3 antibody titer dilutions changed (P = 0.001) over the length of the study. Ewe BW change, serum alkaline phosphatase activity, and liver Zn concentrations did not differ (P > 0.22) between 0Zn and +Zn or 0vitE and +vitE ewes. Serum a-tocopherol tended to be higher (P = 0.08) in +vitE than 0vitE ewes and was numerically higher (P = 0.16) in +Zn than 0Zn ewes. Antibody titer dilutions were higher (P = 0.06) in 0Zn than +Zn ewes and did not differ (P = 0.83) between 0vitE and +vitE ewes. These results indicate that high levels of supplemental Zn may have a tendency to improve serum alpha-tocopherol concentrations but may have negative impacts on humoral immune function.