Studies on the assimilation and storage of copper in crossbred sheep.

1954 ◽  
Vol 5 (3) ◽  
pp. 511 ◽  
Author(s):  
AT Dick
Keyword(s):  
Copper Metabolism ◽  
Copper Accumulation ◽  
Sulphate Content ◽  
Nickel Iron ◽  
Liver Copper ◽  
Number Of Factors ◽  
Inorganic Sulphate ◽  
Copper Storage ◽  
Experimental Findings ◽  
And Storage

Experiments reported in this paper show that increased copper intake of sheep is reflected by increased copper content of the liver. The magnitude of the rise in liver copper depends upon a number of factors, but under the described conditions, the amount of copper accumulated by the animal is proportional to the copper intake within the range 3-20 mg per day; the amount stored in the liver over a 6 months1 period was found to be 4.5-5 per cent. of the intake. Some of the conditions which may modify the retention of copper were examined. It was found that the addition of ferrous sulphide to the diet, which presumably converts added copper to the insoluble sulphide, lowered the expected copper accumulation in the liver by 75 per cent. Conditions which may modify this effect of ferrous sulphide have been examined and described. Other possible sources of sulphur for the formation of copper sulphide in the animal (elemental sulphur, sodium thiosulphate) were found not to be effective. The effects of some other metals (zinc, nickel, iron, and molybdenum) on copper accumulation in the liver were examined. Molybdenum was found to have a severely limiting effect, but this effect was only observed when the diet also contained a sufficient quantity of inorganic sulphate. For a given intake of molybdenum the limitation of copper storage was found to be proportional to the sulphate content of the diet. The possible bearing of these experimental findings on conflicting field observations relating to copper metabolism of sheep is discussed.

Effect of chelators on copper metabolism and copper pools in mouse hepatocytes

1989 ◽  
Vol 256 (4) ◽  
pp. G667-G672
Author(s):  
H. J. McArdle ◽  
S. M. Gross ◽  
I. Creaser ◽  
A. M. Sargeson ◽  
D. M. Danks
Keyword(s):  
Metal Ion ◽  
Chelation Therapy ◽  
Copper Metabolism ◽  
Copper Accumulation ◽  
Copper Uptake ◽  
Mouse Hepatocytes ◽  
Copper Chelators ◽  
Copper Storage ◽  
And Storage

Disorders of copper storage are usually treated by chelation therapy. It is generally thought that the chelators act by mobilizing copper from the liver, hence allowing excretion in the urine. This paper has examined the effect of chelators on copper uptake and storage in mouse hepatocytes. Penicillamine, a clinically important chelator, does not block the uptake of copper or remove copper from hepatocytes. Two other copper chelators, sar and diamsar, which form very stable and kinetically inert Cu2+ complexes by encapsulating the metal ion in an organic cage, were shown to block copper accumulation by the cells and to remove up to 80% of cell-associated copper. They also removed most (approximately 80%) of the 64Cu accumulated by the cells in 30 min, but released only a small percentage (less than 20%) of that accumulated over 18 h. The results show that copper in the hepatocyte can be divided into at least two pools, an easily accessible one, and another, not removable even after long-term incubation with any of the chelators. Most of the copper normally found in the cell appeared to be associated with the former pool.

Observations on the copper metabolism of the domestic fowl and duck.

1961 ◽  
Vol 12 (4) ◽  
pp. 743 ◽  
Author(s):  
AB Beck
Keyword(s):  
Copper Sulphate ◽  
Domestic Fowl ◽  
Copper Concentration ◽  
Copper Metabolism ◽  
Basal Diet ◽  
Moderate Increase ◽  
Dietary Copper ◽  
Liver Copper ◽  
Copper Storage ◽  
The Relationship

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

Copper-molybdenum-sulphate-manganese interaction and the copper status of cattle

1958 ◽  
Vol 9 (3) ◽  
pp. 373 ◽  
Author(s):  
PJ Mylrea
Keyword(s):  
Manganese Content ◽  
Basal Diet ◽  
Sulphate Content ◽  
Liver Copper ◽  
Copper Status ◽  
South Wales ◽  
Definite Effect ◽  
Inorganic Sulphate ◽  
The Mean ◽  
Low Levels

The influence of molybdenum, inorganic sulphate, and manganese upon the copper status of cattle was investigated. The mean liver copper concentration increased for steers on a basal diet containing 7.6 p.p.m. copper, 2.4 p.p.m. molybdenum, 91 p.p.m. manganese, and 0.03 per cent. sulphate. In steers on a similar diet but with the sulphate content increased to 0.55 per cent., with or without an increase in the manganese content to 391 p.p.m., there was a highly significant reduction (P=0.01) in the liver copper concentrations but not to low levels. There was also a significant (P=0.01) increase in the serum inorganic sulphate levels. On increasing the molybdenum content to 9.2 p.p.m. there was a further reduction, to low levels, in the liver and blood copper concentrations of steers on the high sulphate diets but there was no definite effect on those on the low sulphate diet. Manganese again appeared to be without effect. It was concluded that there was a molybdenum-sulphate interaction with copper in cattle but that, under the conditions of this trial, manganese was without effect. Despite the very low liver and blood copper levels attained, and maintained for 15 weeks, there was no clinical evidence of hypocuprosis. The mineral and sulphate levels applied in some of these treatments are similar to those found in pastures from areas in New South Wales where copper deficiency in cattle occurs. The levels in pastures, as related to the results of this trial, are discussed.

scholarly journals Copper Supplementation, A Challenge in Cattle

Animals ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1890
Author(s):  
Marta López-Alonso ◽  
Marta Miranda
Keyword(s):  
Copper Deficiency ◽  
Copper Toxicity ◽  
Copper Metabolism ◽  
Copper Accumulation ◽  
Hepatic Copper ◽  
Copper Status ◽  
Large Numbers ◽  
Copper Supplementation ◽  
Key Points ◽  
Copper Storage

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.

Copper-molybdenum-sulphate interaction in induction of Ovine hypocupraemia and hypocuprosis

1956 ◽  
Vol 7 (1) ◽  
pp. 45 ◽  
Author(s):  
KN Wynne ◽  
GL McClymont
Keyword(s):  
Basal Diet ◽  
Ammonium Molybdate ◽  
Sodium Sulphate ◽  
Copper Level ◽  
Sulphate Content ◽  
Liver Copper ◽  
South Wales ◽  
Inorganic Sulphate ◽  
The Mean ◽  
Restricted Feed Intake

A basal diet containing 6.2 p.p.m. copper, 0.8 p.p.m. molybdenum, and 0.04 per cent. inorganic sulphate was fed unsupplenlented to one group of sheep. Four other groups were fed on the same diet supplemented with ammonium molybdate to give a molybdenum content of 5.1 p.p.m. or with sodium sulphate to give an inorganic sulphate content of 0.40 per cent., or with both. Sheep on the unsupplemented basal diet showed no marked disturbance of their liver and blood copper concentrations. Sheep maintained for 50 weeks on the diet containing both molybdenum and sulphate supplements showed a progressive fall in liver and blood copper levels, and developed dystrophic wool and hypochromatrichia. On a restricted feed intake of the same diet, sheep displayed a similar fall in liver copper and similar wool changes, but maintained a normal blood copper level for a longer period before developing hypocupraemia. Hypochromatrichia appeared to develop in this group before hypocupraemia was evident. With only the sulphate supplement added to the basal diet, liver copper concentrations fell, but not to a level associated with hypocupraemia. With only the molybdenum supplement added to the basal diet, copper retention by the liver was depressed to a small, but significant extent compared with the controls. The diet of the groups showing evidence of hypocuprosis approximately reproduced the mean copper, molybdenum, and sulphate status of the feed in an area in New South Wales enzootically affected with hypocuprosis. It is concluded that hypocuprosis in this area at least is explicable in terms of copper-molybdenum-sulphate interaction.

A Perspective on Copper and Liver Disease in the Dog

2000 ◽  
Vol 12 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Larry P. Thornburg
Keyword(s):  
Liver Disease ◽  
Storage Disease ◽  
Copper Metabolism ◽  
Normal Liver ◽  
Clinical Problem ◽  
Normal Function ◽  
Copper Accumulation ◽  
Hepatic Copper ◽  
Copper Storage ◽  
End Stage

Copper is a ubiquitous trace metal necessary for normal function of a variety of cellular proteins. Intracellular copper metabolism is complex, and only a few of the proteins/genes involved are known. Copper deficiency does not appear to be a clinical problem in dogs. Excess copper accumulation in the liver as a cause of hepatitis and cirrhosis was first demonstrated among Bedlington terriers. Subsequently, copper accumulation in the liver has been shown to occur in several other breeds of dogs. Excess hepatic copper has been found in dogs with normal liver histology, dogs with hepatitis, and dogs with end stage cirrhosis. Evidence is accumulating that copper is a cause of liver disease in breeds of dogs other than Bedlington terriers. Moreover, as more data are accumulated, the copper storage disease appears to have characteristics that are very similar among all of the affected breeds.

The copper metabolism of warm-blooded animals with special reference to the rabbit and the sheep

1963 ◽  
Vol 14 (1) ◽  
pp. 129 ◽  
Author(s):  
AB Beck
Keyword(s):  
Special Reference ◽  
Copper Metabolism ◽  
Limited Capacity ◽  
Liver Copper ◽  
Excess Copper ◽  
Real Increase ◽  
Copper Storage

Groups of rabbits were fed for 12 weeks on the same diet at two levels of copper intake (8.5 and 30 p.p.m. Cu). There was no real increase in the liver copper levels at the higher copper intake. When rabbits were injected intravenously with 1 mg Cu, the excess copper was eliminated from the liver in 96 hr. Some copper was excreted through the bile and some appears to have been excreted directly into the caecum. Experiments are described which show that, by contrast, the sheep very slowly lost excess copper from the liver. The rate of loss was the same whether the copper had been given orally or intravenously. The patterns of copper storage and excretion in warm-blooded animals are outlined, and it is postulated that the unusual copper metabolism of the sheep IS due to a limited capacity to excrete excess copper from the liver.

Assessment of copper accumulation in archived liver specimens from cats

2020 ◽  
pp. 1098612X2096135
Author(s):  
Punyamanee Yamkate ◽  
Randi M Gold ◽  
Panagiotis G Xenoulis ◽  
Katja Steiger ◽  
David C Twedt ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Hepatic Steatosis ◽  
Dry Weight ◽  
Reference Interval ◽  
Copper Accumulation ◽  
Zonal Distribution ◽  
Tissue Samples ◽  
Hepatic Copper ◽  
Liver Copper ◽  
Flame Atomic Absorption

Objectives The aim of this study was to assess hepatic copper concentrations and zonal distribution in cat liver specimens. Methods For this study, 121 archived, formalin-fixed, paraffin-embedded liver specimens from cats were used. Tissue sections were stained for copper with rhodanine and scored from 0 (no copper accumulation) to 5 (panlobular copper accumulation). The tissue specimens were then deparaffinized and hepatic copper concentrations were measured using flame atomic absorption spectroscopy. Results Tissue samples were categorized into four groups based on histopathologic findings: (1) no significant histopathologic hepatic changes (n = 66); (2) hepatic steatosis (n = 18); (3) inflammatory or infectious disease (n = 24); and (4) neoplasia (n = 13). Of the 121 specimens, 13 (11%) stained positive for copper, with three having a score ⩾3. Thirty-seven specimens (31%) had copper concentrations above the reference interval ([RI] <180 µg/g dry weight liver). Copper concentrations in cats with hepatic inflammatory or infectious disease were significantly higher than cats with hepatic steatosis ( P = 0.03). Copper-staining score and concentration were positively correlated ( rs = 0.46, P <0.001). Conclusions and relevance Despite the fact that 31% of specimens had copper concentrations above the RI, only 11% showed positive copper staining and only 2.5% had a score ⩾3. Our findings suggest that hepatic copper concentrations greater than the upper limit of the RI are relatively common in cats. Further studies to determine the factors that influence hepatic copper staining in cats and to establish contemporary RIs for hepatic copper in healthy cats are warranted.

Thiomolybdates and the copper–molybdenum–sulphur interaction in ruminant nutrition

1975 ◽  
Vol 85 (3) ◽  
pp. 567-568 ◽  
Author(s):  
A. T. Dick ◽  
D. W. Dewey ◽  
J. M. Gawthorne
Keyword(s):  
Copper Accumulation ◽  
Ruminant Nutrition ◽  
Inorganic Sulphate

In 1945 we reported (Dick & Bull, 1945) the first observations on the effects of molybdenum in the diet of ruminants in limiting the accumulation of copper in their tissues.Further observations (Dick, 1952) indicated that there was a third factor which materially altered the control by molybdenum of copper accumulation and this factor, present in lucerne hay, was identified as inorganic sulphate (Dick, 1953a). It was also shown that sulphate regulated molybdenum excretion (Dick, 1953b) in the urine and hence the level of molybdenum in circulating blood (Dick, 1953c).

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