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

In ruminants, copper is absorbed in the first parts of the intestine. Mainly transported by ceruloplasmin, it concentrates in the liver; then it is eliminated by feces, bile, urine and milk. Copper intoxications are relatively rare. On the contrary, deficiencies are more frequent: they are due to a shortage of alimentary supply or to a competition with molybdenum and/or sulphate. These deficiencies induce the inhibition of copper-enzymes determining mainly troubles of hair pigmentation, reproduction and hematopoiesis. These troubles can be prevented or cured by the administration of copper salts.
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PMID:[Copper in ruminants. Review]. 635 8

Experiments were carried out on 61 male and female Wistar rats. Following 21-day intraperitoneal administration of molybdenum (Na2MoO4 X 2H2O), significant differences in the level of blood serum ceruloplasmin were noted in female rats depending upon the applied dose of molybdenum. In analogous groups of male rats no statistically significant differences were observed, which might indicate that the effect of molybdenum upon enzymatic ceruloplasmin activity is sex-related. The rats on an increased dietary level of 14 ppm molybdenum, of 10.8 ppm copper content and 507 ppm inorganic sulphur, showed decreased blood serum ceruloplasmin activity irrespective of their sex.
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PMID:The effect of molybdenum upon blood serum enzymatic ceruloplasmin activity in rats. 664 8

Of 8 Thoroughbred foals in which osteochondrosis developed before weaning, 7 had serum copper and ceruloplasmin concentrations below normal. Three foals on one farm had serum zinc content high enough to suggest zinc toxicosis, and the liver of each foal contained abnormally high content of zinc. Four foals from the second farm had extremely low serum copper content, but normal serum zinc content. Evidence of environmental exposure to excess zinc was not found on either farm. The lesions in the zones of endochondral ossification of the afflicted foals were similar in many respects to those found in other species of animals with molybdenum-induced copper deficiency and with inhibition of the function of copper-dependent lysyl oxidase by beta-aminopropionitrile, a toxic component of Lathyrus odoratus known to cause osteolathyrism.
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PMID:Considerations of copper metabolism in osteochondrosis of suckling foals. 674 86

1. Twenty heifer calves were allocated to four groups and maintained for 32 weeks on a diet based mainly on barley and straw and containing 4 mg copper/kg. The diet was supplemented with 0 or 800 mg iron/kg and 0 or 5 mg molybdenum/kg. 2. Liver and plasma Cu concentrations, erythrocyte superoxide dismutase (EC 1.15.1.1) and plasma caeruloplasmin (EC 1.16.3.1) activities decreased greatly and rapidly in all calves given the Fe or Mo supplements or both. Levels indicative of severe Cu deficiency were attained within 16 weeks. There were no significant differences in values in animals given Fe, Mo or Fe plus Mo. 3. Clinical signs of Cu deficiency developed after 20 weeks in the calves given the Mo supplement. Growth rates were reduced, skeletal lesions developed and hair texture and colour were affected. No such effects were observed in the calves given only the Fe supplement. 4. Plasma and liver Fe concentrations increased in calves given the Fe supplement but were not greatly affected by Mo, even when the calves were severely Cu-deficient. 5. The significance of the effects of Fe and Mo on Cu metabolism are discussed with special regard to the influence of soil ingestion on Cu availability and to the frequent lack of correlation between the Cu status of animals and their clinical condition.
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PMID:The influence of dietary iron and molybdenum on copper metabolism in calves. 682 92

1. Male WAG/Cpb inbred rats fed on rations containing 1.5 mg copper/kg (deficient) and 6.0 mg Cu/kg (adequate) were supplemented with molybdenum (500 mg/kg diet). Starting at week 0 rats were killed weekly for up to 6 weeks and the caeruloplasmin activity of plasma, the Cu concentration of plasma, liver and kidney and the Mo concentration of liver and kidney were determined. The experiment was repeated with rats fed on diets of the same composition but given additional Cu for periods of 2 weeks. Cu was given orally by increasing dietary Cu to 6.0 mg/kg and 25.0 mg/kg for Cu-deficient and Cu-adequate rats respectively or intraperitoneally by injecting 75 micrograms and 250 micrograms every second day to Cu-deficient and Cu-adequate rats respectively. 2. After Mo administration to Cu-deficient rats plasma and kidney Cu and liver and kidney Mo increased but caeruloplasmin activity and liver Cu decreased. In Cu-adequate rats plasma, liver and kidney Cu and liver and kidney Mo increased to much higher levels than in Cu-deficient rats. Caeruloplasmin activity was not affected. Fluctuations in plasma Cu and kidney Mo were correlated closely. 3. No qualitative difference between the effect of oral or intraperitoneal Cu administered to Mo-treated Cu-deficient or Cu-adequate rats was found. In Cu-deficient Mo-supplemented rats additional Cu increased plasma Cu, caeruloplasmin activity and liver and kidney Cu and Mo. In Cu-adequate Mo-supplemented rats additional Cu decreased plasma Cu and liver and kidney Mo and increased caeruloplasmin activity and kidney cu and, to a minor extent, liver Cu. 4. In veiw of the assumption that in rats a Cu, Mo and S containing compound, related to Cu-thiomolybdate, may be formed in vivo the results suggest that cu binds to the Mo-S part of the compound; when this compound is formed in the gastro-intestinal tract it can not be absorbed and when it is formed at systemic sites it changes the Cu distribution.
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PMID:Changes in the distribution of copper and molybdenum after Mo administration and subsequent additional oral or intraperitoneal Cu administration to rats. 711 61

Values for ceruloplasmin activities and copper concentrations were found to be lower in serum than in paired samples of plasma in both sheep and cattle. Ceruloplasmin activities in serum were 13-40% lower relative to plasma for nine different groups of animals, and 10-65% lower for individual animals (n = 112). As the values are not directly interchangeable, plasma rather than serum should be used when estimating copper nutrition in these animals. Maximum effects in serum were apparent 3-4 h after collection, the earliest time at which serum could be obtained. Lower ceruloplasmin and copper values in serum could not be attributed to the type of blood collection vessel used, subsequent storage of samples, the methods used for measuring ceruloplasmin activities and copper concentrations, the formation of fibrin in blood, or to the effects of dietary molybdenum. In contrast, the addition of neuraminidase to whole blood before clotting decreased the differences between serum and plasma ceruloplasmin activity and copper concentration in a dose-dependent manner. Of the two major copper-containing enzymes present in blood, effects of clotting were only evident with ceruloplasmin. Cu-Zn-containing superoxide dismutase activity in erythrocytes was unaffected by clot formation. The results indicate that ceruloplasmin and the copper associated with this protein are sequestered into the clot during clot formation by attachment of the enzyme to the blood cellular fraction. The minimizing of this effect by the addition of neuraminidase suggests that this attachment may be through sialic acid residues.
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PMID:Differences between serum and plasma ceruloplasmin activities and copper concentrations: investigation of possible contributing factors. 715 92

In copper-deficient lambs with serum copper less than 0.30 microgram/ml there was a linear relationship between erythrocyte superoxide dismutase (SOD) activity and serum copper concentration. When these lambs were fed adequate copper (10-14 mg/kg of feed), SOD increased by 68 per cent over 90 days. The time course of this increase corresponded to the erthrocyte lifespan of lambs. In sheep given excess copper (0.25 g/kg body weight over seven weeks) erythrocyte SOD activity did not differ significantly from that of control sheep. A 40 per cent decrease in erythrocyte SOD activity occurred in sheep fed diets supplemented with molybdenum and sulphate for 90 days. Compared with controls, these sheep stored less copper in their livers and had similar caeruloplasmin activities but higher serum copper concentrations.
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PMID:Effects of changes in nutritional copper on erythrocyte superoxide dismutase activity in sheep. 737 20

1. Male WAG/Cpb inbred rats fed on rations with approximately 1.5 mg copper/kg (deficient), 6.0 mg Cu/kg (adequate) and 25.0 mg Cu/kg (excess) were supplemented with varying amounts of molybdenum (0, 50, 150 and 500 mg/kg diet) and the effect on the Cu concentration of blood, plasma, liver and kidney, the caeruloplasmin activity of plasma and the Mo concentration of liver and kidney were studied. 2. Mo increased the Cu concentration of blood, plasma, liver and kidney and the Mo concentration of liver and kidney. 3. In the plasma of Mo-supplemented rats the presence of a Cu-containing fraction was demonstrated, the Cu of which did not react with dithiocarbamate and was not related to caeruloplasmin. The Cu in this fraction was not able to increase the caeruloplasmin activity in the plasma of Cu-deficient Mo-supplemented rats. The Cu concentration of the erythrocytes did not seem to have been increased by the Mo treatment. 4. When compared to Cu-adequate rats the effect of Mo on the Cu distribution was reduced both by Cu deficiency and Cu excess. This decreased effect of Mo was explained by reduced uptake or retention of Mo in the body as observed in the liver and kidney.
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PMID:The influence of molybdenum on the copper metabolism of the rat at different Cu levels of the diet. 737 40

Molybdenum, as ammonium molybdate, was added to the drinking water of 5-wk-old calves to establish the minimum toxic concentration. A basal diet with 13 ppm copper and .29% sulfur was fed ad libitum for 21 days. The concentration of copper in liver was reduced with 50 ppm added molybdenum in water but not with 1 or 10 ppm. However, copper in plasma was elevated with 50 ppm added molybdenum in water while changes in ceruloplasmin concentration were nonsignificant. The calculated percent copper as ceruloplasmin copper in plasma decreased from 61% to 43% with all additions of molybdenum. Apparently uptake of plasma copper by tissues was reduced by molybdenum decreasing the bioavailability of copper. These data indicate the difficulty of detecting molybdenum-induced hypocuprosis from plasma copper and ceruloplasmin without data on tissue copper. With dietary levels of 13 ppm copper and .29% sulfur, the minimum toxic concentration of molybdenum in drinking water for calves is between 10 and 50 ppm, and the critical copper-to-molybdenum ratio is less than .5. Molybdenum in water may be less toxic to calves than molybdenum in fresh forages.
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PMID:Toxicity of ammonium molybdate added to drinking water of calves. 738 Oct 83

Three groups of ten young ewes (29 kg) received a basal diet or a diet enriched in sulphur (3 g/kg DM) or sulphur (3 g/kg DM) plus molybdenum (13 mg/kg DM). The total plasma copper increased in the S + Mo group. The trichloracetic acid (TCA) insoluble copper fraction of this group rose sharply from the second week of experiment. A decrease in ceruloplasmin oxidase activity could be detected in non-saturating or saturating substrate conditions in the enzyme assay, either with paraphenylenediamine or o-dianisidine as substrate. It was concluded that the decrease was due to failure of synthesis rather than inhibition. The plasma TCA insoluble copper fraction is thus the earliest and most reliable parameter for molybdenosis diagnosis in sheep.
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PMID:Biochemical parameters useful for the diagnosis of mild molybdenosis in sheep. 745 38


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