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

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.

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


1954 ◽  
Vol 5 (3) ◽  
pp. 511 ◽  
Author(s):  
AT Dick

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.


1996 ◽  
Vol 17 (12) ◽  
pp. 448-448
Author(s):  
Philip O. Ozuah

Wilson disease (hepatolenticular degeneration) is an autosomal recessive, inherited disorder of copper metabolism resulting in excessive accumulation of copper in the liver, brain, and other organs of the body. The manifestations of the disease are related directly to this accumulation of copper. Copper homeostasis normally is a product of the balance between intestinal absorption of dietary copper and hepatic biliary excretion of excess copper. In Wilson disease, incorporation of hepatic copper into ceruloplasmin is defective and excretion of copper in the bile is reduced. A low level of ceruloplasmin, which until a few years ago was erroneously considered to be the basis for the disease, is a consequence of the underlying metabolic defect.


1967 ◽  
Vol 18 (1) ◽  
pp. 169 ◽  
Author(s):  
GI Alexander ◽  
JM Harvey ◽  
JH Lee ◽  
WC Stubbs

Four experiments described determined the effect of copper and cobalt therapy on the growth and productivity of cattle on the marine plains of central coastal Queensland. Copper was administered by subcutaneous injections of copper glycinate, and cobalt by dosing per os with heavy cobalt pellets. The growth of weaned cattle was significantly improved by copper, particularly from June to October when limited palatable feed on the high ground forced the animals to forage on the para grass swamps. During the same period, 2-year-old heifers also showed a growth response to copper. Their conception rate increased after 19 months of copper therapy but not after 10.5 months. The growth rate of their calves bas significantly increased by copper supplementation. Liver copper concentrations were always low in untreated cattle. Copper therapy maintained these reserves at higher levels, which varied according to the season and the rate of growth of the animals. Calves born to treated cows had higher initial liver copper reserves than those from untreated cows, but in the absence of copper therapy these reserves declined to low and comparable levels in all calves at weaning. Pasture analyses suggest that the copper deficiency revealed was due to interference with copper metabolism rather than to a low copper status in the diet; this interference did not appear to be due to molybdenum. Weaned cattle appeared to respond to cobalt during 1960 but not subsequently, while the cows and calves showed no response. The vitamin B12 status in liver and serum appeared adequate in both treated and untreated cattle.


Hepatology ◽  
1986 ◽  
Vol 6 (3) ◽  
pp. 427-432 ◽  
Author(s):  
Surjit K. S. Srai ◽  
Andrew K. Burroughs ◽  
Bernard Wood ◽  
Owen Epstein

1979 ◽  
Vol 19 (98) ◽  
pp. 312 ◽  
Author(s):  
EB Greer ◽  
CE Lewis ◽  
MG Croft

The effects of supplementing a wheat/animal protein diet with copper (nil, 125 or 250 ppm), zinc (nil or 150 ppm) and iron (nil or 150 ppm) were studied in a 2 x 2 x 2 x 3 factorial experiment with 48 pigs. The diet was restrictively and individually fed to barrows and gilts between 18 and 73 kg liveweight. Daily rate of gain, feed conversion ratio and carcase score were not affected by the supplementary minerals. Supplementary copper increased the storage of manganese, zinc and copper in the liver. Although liver copper levels were greater in both sexes at 250 than at 125 ppm copper, barrows stored more copper than gilts at the higher level. Adding 150 ppm zinc at the same time as 250 ppm copper reduced liver copper storage in the barrows to the level of that in gilts given the same amount of copper. The iodine number, i.e, softness, of backfat in barrows was increased to that of gilts by 250 ppm copper; gilts were unaffected. Zinc supplementation also increased backfat softness in barrows but not in gilts. Despite this, 150 ppm zinc partially reduced the effect of 250 ppm copper on backfat in barrows.


1961 ◽  
Vol 3 (1) ◽  
pp. 89-95 ◽  
Author(s):  
D. B. Bellis

A trial has been carried out to determine the effects of supplementing bacon pig diets with 125 and 250 ppm. copper (as copper sulphate) and/or aureomycin (14·4 ppm.). A total of 288 pigs were fed ad lib. from 40·100lb., and restricted-fed thereafter to bacon weight (200 1b.). Growth rate was increased by 125 ppm. copper, 250 ppm. copper, and aureomycin during the ad lib. feeding period. The magnitude of the responses was about the same in each case.During the fattening stage from 100 1b. to bacon weight, 125 ppm. copper or aureomycin increased food conversion efficiency; 250 ppm. copper however improved growth rate also. There was probably some additive effect of 125 ppm. copper and aureomycin when fed together, but it is unlikely that such an effect occurred with the higher level of copper and aureomycin.The liver copper content of pigs fed 125 ppm. copper was 3 times higher than that of the controls; 250 ppm. copper increased liver copper storage about 18·fold.The similarity in response of copper and aureomycin feeding to pigs is discussed. It is concluded that, under the conditions of the trial, their mode of action is similar. Under similar conditions in general farm practice there is unlikely to be any economic advantage in supplementing pig diets containing 250 ppm copper with aureomycin; however, the bacterial environment may sometimes be such that additional benefit will be obtained by joint supplementation.


1982 ◽  
Vol 204 (2) ◽  
pp. 541-548 ◽  
Author(s):  
J E Balthrop ◽  
C T Dameron ◽  
E D Harris

Soluble fractions from chick liver and aorta were examined for copper-binding proteins. In liver a zinc-binding thionein appeared to be the major binding protein for copper. Aortic tissue contained only traces of this thionein protein. Unlike liver, moderate amounts of soluble copper in aorta showed no association with macromolecules. Chicks fed on copper-deficient diets for 8 days had one-third the liver copper concentrations of controls. Aortic copper concentration was decreased only slightly, but the activity of lysyl oxidase, a copper-dependent enzyme in aorta, was decreased significantly. Treating the deficient chicks with CuSO4 (1 mg/kg) restored liver copper rapidly. The increase correlated with the binding of copper to a 10 000-mol.wt. component in the soluble fraction. Aortic copper concentrations responded much less to the CuSO4 treatment, but lysyl oxidase activity was again measurable in the tissue. Radioactive isotopes of copper bound almost exclusively to the 10 000-mol.wt. component in liver and to components of mol.wt. 30 000 or above in aorta. Hardly any of the administered radioactivity appeared with the 10 000-mol.wt. components in aorta, and none was found with unbound copper. The 30 000-mol.wt. components in aorta showed superoxide dismutase activity that was sensitive to NaCN. They also showed the highest specific activity of copper of any other aorta component. A clear distinction was seen between the metabolism of copper in liver and aortic tissues. Whereas a copper thionein, metallothionein, was a major component in the liver pathway, it is doubtful that this protein plays a major role in the intracellular metabolism of copper in aortic tissue.


2021 ◽  
Vol 22 (1) ◽  
pp. 49-55
Author(s):  
J. A. AGUNBIADE ◽  
G. M. BABATUNDE

The study which lasted 3 months was a factorial arrangement in which nine dietary treatments resulting from supplementation of a commercial layers diet with 0, 200 or 400 mg/kg Copper and 0, 100 or 200 mg/kg Iron were fed to 135 fifty two-week old laying hens of the Golden Hubbard Connect Strain. After 12 weeks on the diets, three birds, randomly selected from each treatment, were slaughtered and their blood, liver, spleen and heart analysed for effect of supplementary copper and iron on haemoglobin content, packed cell volume and weights of the liver, spleen and heart and their copper and iron concentrations. No significant effects of supplementary copper or Iron or their interaction were observed on haemoglobin, packed cell volume or weights of the liver, spleen and heart. However, dietary iron supplementation produced significant (P<0.05) effects on iron storage in the liver and spleen but not on copper storage. On the other hand, copper addition significantly (P<0.05) increased liver storage of copper and spleen storage of iron. Supplementary copper and iron Interaction effects which were not significant for all other measurements, were observed to be significant (P<0.05) for liver copper and Iron concentrations and spleen copper concentration and highly significant (P<0.01) for spleen iron concentration.


1989 ◽  
Vol 256 (4) ◽  
pp. G667-G672
Author(s):  
H. J. McArdle ◽  
S. M. Gross ◽  
I. Creaser ◽  
A. M. Sargeson ◽  
D. M. Danks

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.


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