Copper status of sheep grazing pastures fertilized with sulfur and molybdenum

1981 ◽  
Vol 32 (3) ◽  
pp. 479 ◽  
Author(s):  
JP Langlands ◽  
JE Bowles ◽  
GE Donald ◽  
AJ Smith ◽  
DR Paull

Varying quantities of sodium molybdate, superphosphate and copper sulfate were applied to 30 plots, and changes in hepatic copper concentration in sheep grazing these plots were measured by using a biopsy technique. A relationship between changes in hepatic copper storage and the copper and sulfur x molybdenum concentrations in the green forage on offer was calculated. This relationship was used to calculate the quantity of copper in green forage on offer necessary to maintain hepatic copper concentration constant when the forage varied in sulfur and molybdenum concentration. In a second experiment sodium molybdate was applied to pasture grazed by sheep at rates varying from 0 to 2000 g molybdenum per ha. Black sheep grazing pasture dressed with 2000 g molybdenum per ha, grew white wool for four months following molybdenum application; this corresponded to the period when molybdenum concentration in herbage on offer was greatest. There were also changes in blood, wool, kidney and liver composition following molybdenum application but these were small when molybdenum was applied at the usual commercial rate. The results of both experiments suggest that the application of molybdenum to pasture at commercial rates is unlikely to induce copper deficiencies in grazing sheep.

1983 ◽  
Vol 34 (6) ◽  
pp. 751 ◽  
Author(s):  
JP Langlands ◽  
JE Bowles ◽  
GE Donald ◽  
AJ Smith ◽  
DR Paull ◽  
...  

In a series of experiments aimed at evaluating copper oxide as a supplement, grazing sheep were dosed with varying quantities of copper oxide particles up to 64 g, and the toxicity, the rate of particle excretion, and copper storage in the liver and other tissues were recorded. The toxicities (LD50) of copper oxide particles were 1.17 and 1.80 g/kg liveweight for two groups of grazing adult fine-wool Merino sheep. Death usually occurred 88-96 days after the oral administration of the particles; mean hepatic copper concentrations of sheep dying from copper toxicity were 4122-4308 mg/kg DM. The rate of faecal copper excretion of copper-supplemented sheep, expressed as a percentage of the dose, was less when 50 g of particles were given than when the dose was 5 or 10 g, but excretion patterns were variable. The quantity of hepatic copper stored per g of copper oxide given declined as the dose increased from 0 to 32 g, but increased again at higher doses. Hepatic copper concentration reached a maximum 2-3 months after dosing and the rate of decline was positively related to dose rate; thus, large doses of copper are unlikely to extend the period of elevated copper status. Large doses also increased whole blood copper concentrations and elevated plasma aspartate transaminase activities; this was taken to indicate copper poisoning. Tissue copper concentrations from sheep given up to 64 g particles are reported; liver was the most sensitive to copper treatment. Copper contents of the lung and kidney also responded to copper therapy, but carcass components such as leg, shoulder and muscle did not. Weaned lambs given 2 g of particles (c. 0.13 g/kg liveweight) grew significantly faster than unsupplemented lambs. This dose rate was approximately one-seventh of that predicted to cause 5% mortality, and it is concluded that, at appropriate dose rates, this method of supplementation did not increase mortality or cause excessive increases in tissue copper concentrations, and could increase growth rate.


Animals ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1890
Author(s):  
Marta López-Alonso ◽  
Marta Miranda

Ensuring adequate copper supplementation in ruminants is a challenging task due to the complexity of copper metabolism in these animals. The three-way interaction between copper, molybdenum and sulphur (Cu-Mo-S) in the rumen makes ruminants, particularly cattle, very susceptible to suffering from secondary copper deficiency. Paradoxically, excessive copper storage in the liver to prevent deficiency becomes a hazard when ruminants are fed copper-supplemented diets even slightly above requirements. While cattle were traditionally thought to be relatively tolerant of copper accumulation, and reports of copper poisoning were until recently somewhat rare, in recent years an increased number of episodes/outbreaks of copper toxicity in cattle, particularly in dairy cattle, have been reported worldwide. The growing number of lethal cases reported seems to indicate that copper intoxication is spreading silently in dairy herds, urging the development of strategies to monitor herd copper status and improve farmers’ awareness of copper toxicity. In fact, monitoring studies carried out on numerous samples collected from culled animals in slaughterhouses and/or diagnostic laboratories have demonstrated that large numbers of animals have hepatic copper concentrations well above adequate levels in many different countries. These trends are undoubtedly due to copper supplementation aimed at preventing copper deficiency, as dietary copper intake from pasture alone is unlikely to cause such high levels of accumulation in liver tissue. The reasons behind the copper overfeeding in cattle are related both to a poor understanding of copper metabolism and the theory of “if adding a little produces a response, then adding a lot will produce a better response”. Contrary to most trace elements, copper in ruminants has narrow margins of safety, which must also be formulated considering the concentrations of copper antagonists in the diet. This review paper aims to provide nutritionists/veterinary practitioners with the key points about copper metabolism in cattle to guarantee an adequate copper supply while preventing excessive hepatic copper loading, which requires à la carte copper supplementation for each herd.


1986 ◽  
Vol 23 (2) ◽  
pp. 148-154 ◽  
Author(s):  
L. P. Thornburg ◽  
D. Shaw ◽  
M. Dolan ◽  
M. Raisbeck ◽  
S. Crawford ◽  
...  

Histologic, histochemical and atomic absorption studies on liver tissue from 71 West Highland white terriers are reported. Twenty-seven dogs had histologically normal liver and copper concentration comparable to mongrel control dogs. Forty-four dogs had hepatic copper concentrations up to 22 limes the mean copper concentration found in clinically normal mongrel dogs. Hepatitis, hepatic necrosis and cirrhosis were associated with the increased copper concentration in some dogs. Matings between dogs with high liver copper concentration produced pups with high liver concentration. The copper storage defect is inherited.


1978 ◽  
Vol 58 (3) ◽  
pp. 525-529 ◽  
Author(s):  
J. E. MILTIMORE ◽  
C. M. KALNIN ◽  
J. B. CLAPP

Cattle fed ad libitum a mixture of salt containing 0.5% copper as copper sulfate had an average increase in Cu concentration from 111 to 328 ppm on a dry weight basis in liver biopsy samples over a 333-day test period. The alfalfa hay ration contained an average of 8.2 ppm Cu and a relatively high copper to molybdenum ratio of 3.9:1. Copper supplementation from a variety of sources was given orally or by injection in an 87-day test. Chelated Cu was compared with Cu in copper sulfate, both mixed with salt, and with Cu injected as Cu calcium edetate. The ration of mixed alfalfa and grass contained 6.9 ppm Cu with sufficient sodium molybdate added to produce a Cu/Mo ratio of unity against which the various Cu sources were tested. There was no significant (P < 0.05) effect of Cu source on Cu storage in the liver. There were no trends (P < 0.10) for chelated Cu to result in higher levels of Cu in the liver than when Cu was supplied as copper sulfate even when chelated Cu was fed as fivefold the recommended levels.


1982 ◽  
Vol 243 (3) ◽  
pp. G226-G230 ◽  
Author(s):  
L. C. Su ◽  
S. Ravanshad ◽  
C. A. Owen ◽  
J. T. McCall ◽  
P. E. Zollman ◽  
...  

Eleven Bedlington terriers were found to have a mean hepatic copper concentration of 6,321 micrograms/g dry wt (normal, 200 micrograms/g dry wt) and renal copper concentration that was three or four times normal. Brain copper levels were normal in younger dogs, were elevated in two older dogs, and were 100 times normal in one dog that died of the disease. Increased concentrations of copper in the liver, kidney, and brain also characterize Wilson's disease. Erythrocyte survival was normal in three affected dogs, but serum glutamic-pyruvic transaminase levels were usually elevated. Unlike the hypoceruloplasminemia of patients with Wilson's disease, plasma ceruloplasmin activity was not only normal but was also slightly elevated in the terriers. Despite their normal or excessive ceruloplasmin, the Bedlington terriers could convert ionic 64Cu to radioceruloplasmin but did so only very slowly. These dogs accumulated significantly more 64Cu in their livers than normal, much like patients with Wilson's disease do before symptoms develop.


1968 ◽  
Vol 8 (35) ◽  
pp. 679 ◽  
Author(s):  
RJW Gartner ◽  
JG Young ◽  
PM Pepper

A 2 X 2 factorial design was used to investigate the effects of copper and cobalt therapy of Hereford steers grazing Lotononis-Pangola pastures on the wet heath areas of coastal south-eastern Queensland. Copper was given as a subcutaneous injection of copper glycinate and cobalt as an intra- ruminal cobalt oxide pellet. Liver samples were obtained at three-monthly intervals for 18 months. The liver copper concentration of untreated animals decreased to low levels (<10 p.p.m.). Copper therapy increased (P<0.01) and cobalt therapy decreased (P<0.01) liver copper levels. There were, however, no significant differences in bodyweight gains.


1994 ◽  
Vol 266 (5) ◽  
pp. G907-G913 ◽  
Author(s):  
M. L. Schilsky ◽  
R. J. Stockert ◽  
I. Sternlieb

Metabolic studies with 67Cu were undertaken to identify the site of the cellular defect in copper metabolism in the Long-Evans Cinnamon (LEC) rat. The apparent rate of copper uptake by LEC primary hepatocytes was increased [maximal velocity (Vmax) = 259 pmol.min-1.mg protein-1] compared with controls (Vmax = 161 pmol.min-1.mg protein-1); however, Michaelis-Menten constant (Km) values were comparable (11.8 and 12.7 microM, LEC and control, respectively). Efflux of copper from LEC and control hepatocytes was similar from 0 to 15 min, but was reduced from 15 to 60 min in the former. Although hepatic copper contents were markedly elevated in LEC rats compared with controls (658 +/- 199 vs. 21.5 +/- 6.6 micrograms/g dry wt), biliary copper concentration was reduced in LEC rats compared with controls (0.187 vs. 1.39 +/- 0.66 microgram/ml). Subcellular fractionation of LEC liver homogenates revealed approximately 75% of copper to be present in cytosol, with gradients of copper concentration from cytosol to either lysosome or microsomal subcellular fractions. LEC rat bile and hepatic microsome and lysosome fractions contained smaller fractions of 67Cu administered intravenously as cupric acetate compared with control rats. However, recovery of 67Cu in bile and in lysosomal subcellular fractions were similar for LEC and controls following administration of 67Cu-labeled asialoceruloplasmin, which is targeted to lysosomes. This discordance suggests a possible defect in the entry of copper into lysosomes but normal delivery of lysosomal copper to bile. Based on these findings, we conclude that the mutation in LEC rats alters copper transport at more than one cellular site.


1961 ◽  
Vol 12 (4) ◽  
pp. 743 ◽  
Author(s):  
AB Beck

Experiments have been carried out to determine whether the concentration of copper in the liver of the domestic fowl and duck can be raised by a moderate increase of dietary copper. Groups of both species were fed for 12 weeks on the same basal diet, to which was added copper sulphate to increase the copper intake two- and fivefold. No significant increase in the liver copper concentration was noted in either species. When copper was administered to both species by intravenous injection, it was rapidly excreted. mostly in the bile. In the fowl a significant amount was excreted through the caeca, but the experiments did not suggest that these organs were important in controlling copper storage. 5tudies on the relationship between h e r copper storage and age showed that there was a rapid increase in the duck after 3 weeks of age. No such changes were observed in the foul


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