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Effects of graded levels of dietary copper on copper and iron concentrations in swine tissues.

In a dose-response study, 120 weanling, crossbred pigs were used to determine the effect of 7.5, 15, 30, 60, 120 and 240 ppm total dietary Cu on animal performance and Cu and Fe stores in selected tissues. Pigs were killed at 56 or 91 kg average body weight. Average daily gain was not affected by dietary treatment. Dietary Cu concentrations of 7.5, 15, 30 and 60 ppm had no appreciable effect on Cu and Fe concentrations in liver and kidney of pigs slaughtered at 91 kg. However, 120 and 240 ppm dietary Cu increased (P less than or equal to .01) liver Cu 4.5- and 16-fold and decreased (P less than or equal to .05) liver Fe by 50 and 60%, respectively, compared with the other dietary treatments. A fit of liver Cu and Fe data to linear plateau models resulted in an inflection point of approximately 60 ppm dietary Cu. Kidney Cu was also increased (P less than or equal to .05) by 120 and 240 ppm dietary Cu, but the magnitude of the change was smaller than that of liver Cu. Muscle Cu and Fe were not significantly affected by dietary Cu.

Animals↗

Influence of molybdenum and sulfate supplementation and withdrawal of diets containing high copper broiler litter on tissue copper levels in ewes.

Thirty-six mature, nongestating, crossbred ewes were allotted randomly to three diets for 140 d: basal (six ewes); 50% basal and 50% broiler litter, dry basis (24 ewes) and 50% basal and 50% deep stacked broiler litter with the addition of 25 ppm molybdenum (Mo) and 5 g sulfate (SO4)/kg feed (six ewes). The control diet and the broiler litter contained 8 and 257 ppm Cu, dry basis, respectively. Liver samples from six ewes in each group were obtained by biopsy initially and at 40, 80 and 120 d and at slaughter (140 d). The remaining 18 litter-fed ewes were fed the basal diet after 140 d and six were slaughtered after 30-, 60- and 120-d. Liver Cu content continually increased (P less than .01) by feeding broiler litter (404 vs 1,543 ppm, dry basis), and was decreased (962 ppm) by supplementing Mo and SO4. During the withdrawal period, liver and duodenum Cu levels were not reduced (P greater than .05). A linear increase (P less than .001) in serum glutamic oxalacetic transaminase (SGOT) was observed with time during the withdrawal period. Serum Cu decreased at 30-d withdrawal and increased thereafter (quadratic effect (P less than .05). Hepatic Cu-metallothionein levels increased 15-fold above control values in the litter-fed ewes (P less than .05).

Animal Feed↗

Effect of faunation on ruminal solubility and liver content of copper in sheep fed low or high copper diets.

Naturally fauna-free crossbred rams approximately 5 mo old, 49.3 +/- 1.88 kg live weight, were allotted to four groups. Two groups remained fauna-free, whereas the other two groups were faunated. A diet based on corn silage-soybean meal containing either a low or a high Cu concentration (7 or 15 micrograms/g dry matter) was fed ad libitum to the two groups for 197 d. The rams were killed at the end of the experiment and livers and ruminal contents were analyzed for Cu. Faunated sheep grew faster (P less than .01) and as a group consumed 1.53 kg diet dry matter daily compared with 1.34 for the fauna-free sheep. Faunated sheep had lower final liver Cu concentrations (P less than .01), total liver Cu per unit of Cu intake and ruminal Cu solubilities (P less than .01) when fed both low and high Cu diets. The relative hepatic Cu uptake was higher by rams fed the low Cu than by those fed the high Cu diet. The results are interpreted to show that faunation decreased the availability of Cu in sheep fed a corn silage-soybean meal diet. The magnitude of the effect was independent of the Cu concentration in the diet.

Animals↗

Catecholamines enhance dihydrolipoamide dehydrogenase inactivation by the copper Fenton system. Enzyme protection by copper chelators.

Catecholamines (CAs: epinephrine, norepinephrine, dopamine, L-DOPA, 6-hydroxydopamine) and o-diphenols (DOPAC and catechol) enhanced dihydrolipoamide dehydrogenase (LADH) inactivation by Cu(II)/H2O2 (Cu-Fenton system). The inhibition of LADH activity correlated with Cu(II), H2O2 and CA concentrations. Similar inhibitions were obtained with the assayed CAs and o-diphenols. CAs enhanced HO. radical production by Cu(II)/H2O2, as demonstrated by benzoate hydroxylation and deoxyribose oxidation; LADH counteracted the pro-oxidant effect of CAs by scavenging hydroxyl radicals. Captopril, dihydrolipoamide, dihydrolipoic acid, DL-dithiothreitol, GSSG, trypanothione and histidine effectively preserved LADH from oxidative damage, whereas N-acetylcysteine, N-(2-mercaptopropionylglycine) and lipoamide were less effective protectors. Catalase (though neither bovine serum albumin nor superoxide dismutase) protected LADH against the Cu(II)/H2O2/CAs systems. Denatured catalase protected less than the native enzyme, its action possibly depending on Cu-binding. LADH increased and Captopril inhibited epinephrine oxidation by Cu(II)/H2O2 and Cu(II). The summarized evidence supports the following steps for LADH inactivation: (1) reduction of LADH linked-Cu(II) to Cu(I) by CAs; (2) production of HO. from H2O2 by LADH-linked Cu(I) (Haber-Weiss reaction) and (3) oxidation of aminoacid residues at the enzyme active site by site-specifically generated HO. radicals. Hydrogen peroxide formation from CAs autoxidation may contribute to LADH inactivation.

3,4-Dihydroxyphenylacetic Acid↗

Effect of copper loading of preruminant calves on intracellular distribution of hepatic copper, zinc, iron, and molybdenum.

The subcellular distribution of Cu, Zn, Fe, and Mo was investigated in liver homogenates from preruminant calves fed control Cu (10 ppm), high Cu (1000 ppm), or high Cu plus high Zn (1000 ppm) milk replacer. For controls, Cu was located primarily in the nuclei and large granule fractions, Zn mainly in the cytosol, and Fe in the cytosol and nuclei fraction; Mo was present in all compartments but least in microsomes. Calves fed high Cu had markedly increased hepatic Cu concentration in the nuclei and cytosol fractions, reduced cytosol Zn, increased nuclei Fe, and decreased Mo concentration in all cell compartments. Feeding high Zn with high Cu (which prevented deaths from high Cu) reversed some changes in hepatic trace element patterns caused by high Cu while initiating new alterations. The marked increase in hepatic Cu and reduced Mo in nuclei and cytosol after Cu loading indicate that these compartments may have a predominant role in the development of Cu toxicity in the preruminant calf.

Analysis of Variance↗

Effects of dietary copper and molybdenum on copper status, cytokine production, and humoral immune response of calves.

Twenty-four male Holstein calves were used to determine the effects of dietary Cu and Mo on performance, Cu status, and immune function of calves. Calves were fed a milk replacer that was deficient in Cu for 8 wk and then were randomly assigned after weaning to one of four treatments: 1) control (no supplemental Cu or Mo), 2) 10 mg of Cu (from CuSO4)/kg of dry matter (DM) (Cu diet), 3) 5 mg of Mo (from Na2MoO4)/kg of DM (Mo diet), or 4) 5 mg of Cu (from CuSO4) and 5 mg of Mo (from Na2MoO4)/kg of DM (Cu + Mo diet). The basal diet was a semipurified diet that contained approximately 1.1 mg of Cu and 1.1 mg of Mo/kg of DM. Calves fed the Cu and Mo diets gained weight more efficiently than those fed the control and Cu + Mo diets during the 112-d study. By d 84 of the study, calves fed the Cu diet had higher plasma Cu concentrations and plasma ceruloplasmin activities than did calves fed the other three diets and had higher liver Cu concentrations on d 136. Plasma and liver Cu concentrations did not differ among calves fed the control, Mo, and Cu + Mo diets. At d 112, activity of Cu-Zn superoxide dismutase was lower in calves fed the Mo diet than in calves fed the Cu diet. Serum total antibodies to porcine erythrocytes (primary response) were lower in calves fed the Mo diet than in calves fed the Cu diet at 7, 14, and 21 d postinoculation. Production of tumor necrosis factor and interleukin-1 by isolated peripheral blood monocytes was not significantly affected by treatment. Although no differences were apparent in plasma or liver Cu concentrations among calves fed the control, Mo, and Cu + Mo diets, calves fed the Mo diet had a more severe Cu deficiency based on depressed humoral immune response and superoxide dismutase activity.

Animals↗