Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.16.3.1 (ceruloplasmin)
 5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical signs of camel sway disease in the Hexi Corridor of Gansu province were defined. The contents of eight minerals in soils, in forage and in the blood and hair of bactrian camels from this region were determined. The related blood indices were also measured. The concentration of molybdenum in soils and forage was 4.8 +/- 0.02 and 4.8 +/- 0.25 micrograms/g (dry matter), respectively, the copper to molybdenum ratio in the forage being only 1.3. The concentration of copper in blood and hair from the camels was 0.28 +/- 0.17 micrograms/ml and 3.50 +/- 1.00 micrograms/g, respectively. There was a hypochromic microcytic anaemia and a low level of ceruloplasmin in the blood. It is therefore suggested that sway disease of bactrian camels in this region is caused by secondary copper deficiency, mainly due to the high molybdenum content in soils and forage. The copper deficiency in the camels was aggravated during reproduction. Oral administration of copper sulphate can prevent and cure the disease.
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PMID:Studies on the relationship between sway disease of bactrian camels and copper status in Gansu province. 783 54

A study was conducted to determine the effects of copper (Cu) depletion by feeding diets high in either iron (Fe) or molybdenum (Mo) on performance and Cu status of beef cows and calves. Thirty-eight 2-yr-old beef heifers, entering the last one-third of gestation, were randomly assigned by expected calving date to one of four diets: 1) control (CON; corn silage-soybean meal-based diet, 4 mg of Cu/kg), 2) control + 600 mg of Fe (as FeCO3)/kg, 3) control + 5 mg of Mo (as Na2MoO4)/kg, and 4) control + 10 mg of Cu (as CuSO4)/kg. From d 28 until after the end of the calving season (d 125), heifers receiving supplemental Cu had higher (P < .05) plasma Cu levels and ceruloplasmin activities than heifers fed the other diets. By d 224, plasma Cu concentrations of heifers fed the CON and Fe diets had increased to levels similar to those observed in the Cu-supplemented heifers, whereas the Mo heifers exhibited the lowest (P < .05) plasma Cu of the four treatments from d 168 through the remainder of the 280-d trial. Plasma Cu concentrations and ceruloplasmin activities were greater (P < .05) in Cu-supplemented than in non-Cu-supplemented calves (diets 1, 2, and 3) from d 168 onward, and the Fe- and Mo-supplemented calves did not differ in either measurement at any time during the trial. Rate of gain did not differ among calves fed the CON, Fe- or Cu-supplemented diets, whereas the Mo-supplemented calves gained at a much slower (P < .05) rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary copper, iron, and molybdenum on growth and copper status of beef cows and calves. 788 33

Plasma Cu concentrations and ceruloplasmin (a Cu metalloenzyme) activity were used to assess relative Cu bioavailability from different Cu sources for growing cattle. In Exp. 1, 18 calves (average BW 207 +/- 7.7 kg) that had been fed Cu-deficient diets since birth were randomly assigned to treatment. Treatments consisted of control (n = 3) or 30 mg/d of supplemental Cu (n = 5/treatment) from Cu oxide (CuO), Cu sulfate (CuSO4), or Cu lysine. Blood samples were obtained for plasma Cu and ceruloplasmin activity on d 0, 7, 14, and 21. Plasma Cu and ceruloplasmin activity were greater (P < .05) on d 7, 14, and 21 for calves supplemented with CuSO4 than for controls. Copper status of calves fed Cu lysine did not differ from that of calves fed CuSO4. Compared with d-0 values, plasma Cu concentrations by d 21 had increased by 95 and 98% in calves supplemented with CuSO4 and Cu lysine, respectively. Copper oxide supplementation did not increase Cu status above that observed in control calves. In Exp. 2, 36 calves (average BW 211 +/- 4.4 kg) were used to compare the relative bioavailability of Cu from CuO and CuSO4 when supplemented to corn silage-based diets high in the Cu antagonists iron (Fe) or molybdenum (Mo). Treatments consisted of no supplemental Cu or 8 mg of supplemental Cu/kg diet from either CuSO4 or CuO. Within each Cu treatment, diets were supplemented with 600 mg of Fe or 5 mg of Mo/kg diet. In calves fed 5 mg of Mo/kg, plasma Cu was lower (P < .05) in those fed no supplemental Cu or CuO compared with calves fed CuSO4 by d 91 and at subsequent sampling dates throughout the 154-d study. Plasma ceruloplasmin activity was decreased (P < .01) by Mo and was increased (P < .05) by CuSO4 compared with CuO. Based on plasma Cu and ceruloplasmin activity, CuSO4 and Cu lysine were similar in bioavailability, but CuO was essentially unavailable.
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PMID:Bioavailability of feed-grade copper sources (oxide, sulfate, or lysine) in growing cattle. 788 34

Six female cattle were given molybdenum (30 ppm) and sulphate (225 ppm) to induce experimental secondary copper deficiency. The total and differential leukocyte numbers and lymphocyte subpopulations were counted and the neutrophil activity was assessed by means of nitroblue tetrazolium reduction and phagocytosis of sheep erythrocytes. The serum caeruloplasmin activity and concentration were also determined. Copper deficiency was confirmed from decreased serum copper levels, the animals with values less than 5.9 mumol/L being considered deficient. Total leukocyte numbers were not affected by the copper deficiency. However, differential counts showed a marked increase in monocyte subpopulations, a significant decrease in B lymphocytes and reduced neutrophil activity. The serum caeruloplasmin activity was decreased about 50%, but the total serum protein concentration was less altered. We concluded that the effect of these changes on the animals' immune competence may contribute to a greater incidence of infectious diseases in copper-deficient cattle.
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PMID:The effect of copper deficiency on the peripheral blood cells of cattle. 954 89

The uptake of tetrathiomolybdate (TTM) by the liver and the removal of copper (Cu) accumulating in the liver in a form bound to metallothionein (MT) by TTM were studied in Long-Evans cinnamon (LEC) rats, an animal model of Wilson disease, in order to develop better treatments for the disease and Cu toxicity. Although molybdenum (Mo) was incorporated in a dose-dependent manner into the livers of both LEC and Long-Evans agouti (LEA) rats, the original strain of LEC rats used as a reference animal, the uptake into the liver of LEC rats was 13 times higher than that in LEA rats. The concentration of Mo in the soluble fraction plateaued and it was distributed more in the insoluble fraction with a higher dose in LEC rats. The concentration of Cu in the whole livers of LEC rats was decreased by TTM in a dose-dependent manner only at lower doses. However, the concentration of Cu in the soluble fraction continued to decrease with the dose of TTM. The results can be explained in terms of complex formation. Namely, TTM forms a complex with Cu, tentatively referred to a Cu/TTM complex, that can be effluxed into the bloodstream, and then binds selectively to albumin when the dose of TTM is low. On the other hand, TTM forms an insoluble complex, named as a Cu/TTM polymer that is precipitated in the liver when the dose is high. The results further indicate that TTM taken up by a cell is immobilized in the cell through the dose-dependent formation of a complex containing Cu, Mo and sulfur (S), which causes further uptake of TTM. TTM injected into rats or incubated in vitro with serum does not remove Cu from ceruloplasmin. TTM is, thus, suggested to target a cell accumulating excess Cu as Cu-MT, and to remove Cu selectively without interacting with Cu in Cu-enzymes. The results indicate that TTM is taken up by the liver depending on the amount of Cu accumulating in the form of MT, and then Cu is effluxed together with Mo in the form of Cu/TTM complex into the bloodstream.
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PMID:Targeting of tetrathiomolybdate on the copper accumulating in the liver of LEC rats. 966 Dec 87

Since the mid-1980s a previously undescribed disease has affected moose in south-western Sweden. Investigations made to reveal evidence of a viral aetiology have proved unsuccessful. Trace element studies in apparently healthy moose shot during regular hunting suggested a trace element imbalance, with excessive molybdenum uptake causing secondary copper deficiency. The results also indicated a possible chromium deficiency. To verify this hypothesis, an experimental study was performed in male goats fed a semi-synthetic diet for 1.5 years. The animals were kept and treated in four groups: Controls, Cu-deficient group (group 1), Cr-deficient group (group 2), and combined Cu- and Cr-deficient group with additional supplementation of tetrathiomolybdate for 10 weeks at the end of the study (group 3). The present paper presents tissue contents of trace and minor elements, haematology and clinical chemical parameters. Feed consumption and weight development, as well as pathological and histopathological investigations, were also performed in this study, but these results are presented elsewhere. Changes in trace element concentrations were determined by comparing groups 1, 2 and 3 with the control group. Increased concentrations were observed for Al, Ca, Co, Fe, Mo, Pb, Se in the liver; for Al, Cd, Co, Cr, Mo in the kidneys; and for Mn and Mo in the ribs. Considerable accumulation of Mn in ribs seems to be a useful way to determine oxidative stress. Decreases in Mg and P in all organs and blood serum is characteristic of Cu deficiency and molybdenosis. Also the ratio of Ca/Mg was increased as the result of tissue lesions causing an intracellular increase in Ca and decrease in Mg. The trace element changes observed in group 1 were enhanced by the Mo supplementation in group 3, resulting in characteristic patterns, 'spectra' of changes. The alterations were not as remarkable in group 2 as in the two other groups. However, Cr deficiency considerably influenced Al, Co, V and to a smaller extent also Mn in ribs. In groups 1 and 2, only a few minor changes were detected in the haematological parameters, probably caused by increased adrenal activity after transportation of the animals. In group 3, severe anaemia was present but also a leukopenia. For the different clinical chemical parameters measured, all three groups showed changes, explained mainly by the altered activity of enzymes induced by trace element deficiencies and imbalance. Impaired carbohydrate and lipid metabolism was seen in groups 1 and 3, with increased concentrations of glucose, lactate and triglycerides in serum. Increased concentrations of total bilirubin were measured in all three groups (bile stasis was also seen post mortem). A considerably increased concentration of serum urea was found in group 3, although there were no indications of renal insufficiency or dehydration. Regarding hormones, a substantial decrease was seen in thyroxine (T4) in group 3 as a result of the molybdenosis, but a minor decrease was also seen in group 1. Insulin on the other hand showed increased levels in group 3--and especially in group 2 due to the Cr deficiency but also affected by the molybdenosis. As could be expected, Cu deficiency (groups 1 and 3) caused low levels of caeruloplasmin, secondarily affecting the Fe metabolism in these animals. Protein abnormalities, detected as altered electrophoretic patterns of serum proteins, were also seen mainly in group 3. The findings were also confirmed by multivariate data analysis, where PCA revealed the overall impact of the deficiencies, and PLS regression coefficients indicated the influence on the various analytes.
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PMID:Experimental copper and chromium deficiency and additional molybdenum supplementation in goats. II. Concentrations of trace and minor elements in liver, kidneys and ribs: haematology and clinical chemistry. 1081 54

The activity of several cuproenzymes in relation to the immune system was examined in serum and blood cells from bovines with molybdenum-induced copper deficiency. Five female cattle were given molybdenum (30 ppm) and sulfate (225 ppm) to induce experimental secondary copper deficiency. Ceruloplasmin activity was determined in serum. The Cu,Zn-superoxide dismutase and cytochrome c oxidase activities were measured in peripheral blood lymphocytes, neutrophils, and monocyte-derived macrophages. Copper deficiency was confirmed from decreased serum copper levels and the animals with values less than 5.6 micromol/L were considered deficient. The content of intracellular copper decreased between 40% and 70% in deficient cells compared with the controls. In copper-deficient animals, the serum ceruloplasmin activity decreased to half of the control value. Both of them, the Cu,Zn-superoxide dismutase and the cytochrome c oxidase activities, undergo a significant reduction in leukocytes, showing differences among diverse cell populations. We concluded that the copper deficiency alters the activity of several enzymes, which mediate antioxidant defenses and ATP formation. These effects may impair the cell immune functionality, affecting the bactericidal capacity and making the animals more susceptible to infection.
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PMID:Cytochrome c oxidase, Cu,Zn-superoxide dismutase, and ceruloplasmin activities in copper-deficient bovines. 1104 17

Copper (Cu) is an essential trace element and constitutes the active center of the redox Cu enzymes such as Cu, Zn-superoxide dismutase (Cu, Zn-SOD), ceruloplasmin and cytochrome c oxidase. Among hereditary diseases due to a defect in the metabolism of Cu, Menkes disease (caused by a Cu deficiency) and Wilson disease (caused by the excessive accumulation of Cu) have been shown to be caused by the mutation of genes encoding Cu-binding ATPase for the efflux of Cu, ATP7A and ATP7B, respectively. Following the identification of these causative genes, intracellular Cu transporters (Cu chaperones) specific for the Golgi apparatus, mitochondria and Cu, Zn-SOD were discovered, and these findings have facilitated the study of the underlying mechanisms of the biological regulation of Cu. Apart from these physiological and biochemical studies, toxicological studies have elucidated the underlying mechanisms of the occurrence of acute hepatitis caused by the accumulation of Cu accumulating in the liver of an animal model for Wilson disease, LEC rats. In these toxicological studies, two biological aspects of metallothionein (MT), i.e., antioxidant and prooxidant depending on the Cu/Zn ratio in Cu-containing MT have been proposed. The present article overviews the recent findings on the biological regulation of Cu and on the toxicological aspect of Cu. It is known that Cu forms a stable ternary complex with molybdenum and sulfur under reductive conditions in the body. On the basis of this observation, tetrathiomolybdate (TTM) has been applied to remove Cu from the liver of Long-Evans rats with a cinnamon-like coat color (LEC) rats. Precise mechanisms underlying the complex formation between Cu bound to MT and TTM were presented, and an appropriate protocol for the chelation therapy was also proposed together with the mechanisms underlying the occurrence of side-effects.
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PMID:[Biological regulation of copper and selective removal of copper: therapy for Wilson disease and its molecular mechanism]. 1108 2

Two studies were conducted to compare the availability of trace minerals offered to Brahman-crossbred heifers in either grain- or molasses-based supplements. Heifers were randomly assigned to bahiagrass pastures of equal size (n = 3 and 2 heifers/ pasture with 6 and 4 pastures/treatment for Experiment 1 and 2, respectively). Two supplements were formulated using corn and cottonseed meal (DRY) or molasses and cottonseed meal (LIQ). In Experiment 2, a third treatment consisted of the DRY supplement with additional S to equal the amount naturally supplied by the LIQ treatment (DRY+S). Supplements were formulated to provide, on average, 1.5 kg of TDN and 0.3 kg of CP/heifer daily and were fed three times weekly. Supplements also were fortified to provide 140, 76, and 63 mg of Cu, Mn, and Zn per heifer daily. Individual heifer weights were collected at the start and conclusion of the study, following a 12-h shrink. Plasma ceruloplasmin and liver Cu, Mn, Mo, Fe, and Zn concentrations were determined on d 0, 29, 56, and 84 in Experiment 1, and d 0, 32, 57, and 90 in Experiment 2. No differences were detected in heifer BW change (-9.3 and -7.3 kg for DRY and LIQ in Experiment 1, and 51.7, 46.3, and 46.7 kg for DRY, DRY+S, and LIQ in Experiment 2, respectively). In both experiments, liver Fe, Mn, and Zn concentrations were not affected by supplement treatment. Molybdenum tended (P = 0.06 and 0.10 for Experiments 1 and 2, respectively) to accumulate in the liver of heifers fed molasses-based supplements. In Experiment 1, Cu accumulation was less (P < 0.001) in heifers fed the liquid supplements (271 vs 224, 286 vs 202, and 330 vs 218 ppm, for DRY and LIQ supplements on d 29, 56, and 84, respectively). In Experiment 2, heifers receiving Cu from DRY supplements had a 155-ppm increase in liver Cu concentration, which was greater (P = 0.03) than DRY+S (87 ppm increase) and LIQ (P < 0.001; 13 ppm increase). Although lower than heifers receiving DRY, heifers receiving DRY+S had greater (P = 0.02) liver Cu concentrations than heifers receiving LIQ by the end of the study. In both experiments, plasma ceruloplasmin concentrations were highest (P < 0.04) in heifers receiving DRY supplement. The results of these studies suggest that components in molasses-based supplements decrease the accumulation of Cu in the liver of beef heifers. The S and Mo components of molasses may be responsible, at least in part, for this antagonism.
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PMID:Effect of corn- vs molasses-based supplements on trace mineral status in beef heifers. 1246 44

The clinical signs of a disorder known locally as "shakeback disease" in yaks in the North of the Qing Hai-Tibetan Plateau of China were defined: they included emaciation, unsteady gait, a 'shivering' back and deprived appetites. Coat colour was not affected. The mineral composition of soil and forages, and samples of blood and hair from yaks in affected ranches in this region were compared with those of 20 samples from unaffected areas. The mean concentration of molybdenum (Mo) in soil and forage was 4.85+/-0.21 and 4.96+/-0.25 microg/g (dry matter), respectively; the mean copper (Cu) to Mo ratio in the forage was only 1.34+/-0.36 compared to 8.12+/-1.31 for unaffected areas. The mean concentrations of Cu in blood and hair from the affected yaks were 0.29+/-0.17 and 3.51+/-1.12 microg/g, respectively, compared with 0.85+/-0.24 and 6.42+/-1.21 microg/g, for controls. The highest value for Cu in the blood of affected yaks was 0.58 mug/g and the lowest 0.03 microg/g (the corresponding highest values for unaffected yaks were 1.03 mug/g, the lowest 0.56 microg/g). There was a hypochromic microcytic anaemia and a low level of ceruloplasmin in the blood. The Cu deficiency in yaks was most severe during pregnancy and lactation, but oral administration of copper sulphate prevented and cured the disease. We conclude that "shakeback disease" of yaks in this region is probably caused by a secondary Cu deficiency, mainly due to the high Mo content in soils and forage.
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PMID:Studies of a naturally occurring molybdenum-induced copper deficiency in the yak. 1649 Jul 20


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