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)

Rheumatoid arthritis (RA) is characterized by low serum Zn and high serum Cu. In multiple linear regression both were explained by disease activity parameters. It is suggested that interleukin-1 causes both changes by 1) increasing the metallothionein-mediated hepatic uptake to serum Zn and 2) upregulating ceruloplasmin (acute phase reactant) gene and synthesis in liver and subsequently the level of ceruloplasmin-Cu complexes in the blood. Cu absorption was diminished by zinc intake. Cu- and Zn-dependent erythrocyte SOD was increased in RA. In contrast to plasma GSHPx serum selenium was low in RA and this was associated with disease activity parameters.
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PMID:Serum zinc, copper and selenium in rheumatoid arthritis. 182 34

The combination of liquid chromatography and inductively coupled plasma/mass spectrometry (ICP/MS) was employed in an exploratory study to determine lead and other trace element species in blood components. In human blood serum, lead was found in at least three molecular weight fractions at greater than 600,000, 260,000, and 140,000. The major part of lead was coincident with the main copper signal at a molecular weight of 140,000. This fraction, binding both copper and lead, was proven to be ceruloplasmin by the application of an immunological reaction prior to chromatographic separation. In rat serum, lead could be detected in four fractions with molecular weights of greater than 600,000, 400,000, 145,000, and 11,000. In human red blood cell hemolysate, the major fraction of lead was found at 250,000, with minor fractions at 140,000 and at 30,000 together with iron in hemoglobin and zinc in carbonic anhydrase. In rat red blood cell hemolysate, lead was detected at greater than 600,000, 145,000, 30,000, and 11,000. Lead isotope ratios were determined in lead binding protein fractions with a precision of +/- 10%. The detection limit for lead in protein fractions was 0.15 micrograms.L-1.
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PMID:Determination of lead and other trace element species in blood by size exclusion chromatography and inductively coupled plasma/mass spectrometry. 182 13

Alterations in zinc (Zn) and copper (Cu) homeostasis have been reported during the acute recovery period following thermal injury in both children and adults. Increased urinary losses of Zn and Cu and decreased plasma concentrations of Zn, Cu, and ceruloplasmin (CP), the major copper transport protein, occur despite adequate provision of these elements in enteral feedings. We now report data for moderately to severely burned children receiving total parenteral nutrition (TPN) supplemented to provide Zn and Cu. Hyperzincuria occurred consistently when 50 micrograms/kg Zn was delivered daily to older children. Similarly, when younger children received 100 micrograms/kg Zn daily, profound hyperzincuria ensued despite a reduction in total plasma Zn. Hypozincemia was accompanied by low levels of Zn in the plasma subfraction normally associated with albumin-bound Zn. The delivery of Cu via TPN was 4-12 micrograms/kg daily, and urinary Cu losses were not elevated. Plasma total Cu and plasma CP were invariably reduced. These findings are discussed in relation to guidelines published for pediatric trace element supplementation during TPN.
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PMID:Zinc and copper status of severely burned children during TPN. 190 24

Plasma zinc, iron, copper, and selenium and selected blood proteins were measured in 66 men before (BHW) and after (AHW) a 5-d period of sustained physical and psychological stress called Hell Week. Recovery blood samples were obtained from 26 men 7 d after Hell Week. Dietary intakes were determined BHW and during Hell Week; zinc, iron, copper, and selenium intakes during Hell Week averaged 23.6 +/- 3.4 mg/d, 35.4 +/- 3.9 mg/d, 3.0 +/- 0.5 mg/d, and 92.5 +/- 26.7 micrograms/d, respectively. C-reactive protein was detected in only five subjects BHW and in all subjects AHW. Zinc, iron, selenium, and albumin decreased by 33%, 44%, 12%, and 9%, respectively, whereas ferritin, ceruloplasmin, and creatine kinase concentrations increased AHW by 59%, 8%, and 266%, respectively. Haptoglobin concentrations increased 57% in 30 subjects but decreased 32% in 23 subjects AHW. The biochemical changes were transitory because protein (except ferritin) and mineral concentrations were similar to BHW values 7 d after Hell Week. Hell Week induced changes characteristic of an acute-phase response in physically active men.
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PMID:Biochemical indices of selected trace minerals in men: effect of stress. 198 37

Wistar rats were exposed to trinitrotoluene (TNT, 200 mg/kg/d x 6 d/wk) for 6 weeks, and a 2-week recovery period was continued after treatment. After initiation of TNT exposure, zinc and copper concentrations in rat testes, liver and serum, and serum caeruloplasmin activity were assayed every 2 weeks. Testicular size and zinc concentrations were decreased throughout the exposure and recovery periods. After 6 weeks of TNT exposure, rat testicular copper and serum zinc concentrations were significantly decreased and increased, respectively. The activities of caeruloplasmin were decreased after 4 and 6 weeks of exposure. Liver zinc and copper concentrations and serum copper concentrations had not changed significantly in rats throughout the exposure and recovery periods. Copper concentration in hair samples from TNT-exposed workers was lower than that in control workers, but zinc content was significantly increased compared with that in control workers.
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PMID:The effects of trinitrotoluene toxicity on zinc and copper metabolism. 200 77

Early response to the exposure of cadmium includes the enhancement in lipid peroxidation with the concomitant impairment in antioxidative defence mechanism. This investigation deals with the delayed response of cadmium induced stimulation of endogenous defence response against its oxidative damage. The administration of cadmium led to an increase in the hepatic enzymatic and nonenzymatic defence armory in a dose dependent manner 72 hrs post its administration. This includes respectively an increase in the activities of superoxide dismutase, glutathione peroxidase, glucose-6-phosphate dehydrogenase and in the levels of glutathione, metallothionein and zinc. Cadmium administration also stimulated serum ceruloplasmin activity in a dose dependent manner. These changes are accompanied by the concomitant decrease in the peroxidative damage to lipids. Our results suggest the development of a delayed adaptive/defence response as a result of exposure to cadmium.
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PMID:Cadmium-mediated induction of cellular defence mechanism: a novel example for the development of adaptive response against a toxicant. 202 6

The toxic milk mutation in mice is an autosomal recessive condition that causes a marked hepatic accumulation of copper in the adults, but is also characterized by severe copper deficiency in the pups of toxic dams. To establish whether the mutation affects ceruloplasmin (CP) gene expression, we analyzed the steady state levels of CP mRNA in mutant and normal animals at various stages of development and following administration of copper and zinc. In fetal and neonatal animals, the expression of the CP gene is unaltered by the mutation or the copper deficiency in the pups of mutant dams. Copper and zinc administration to 7-d-old pups caused a significant increase (35%) in CP mRNA in all genotypes. In the adults that had accumulated 600-700 micrograms/g dry wt of copper in the liver, the CP mRNA level was normal, but pregnancy produced two-to fourfold elevation of the mRNA in both normal and mutant females. These results suggest that the toxic milk mutation does not affect the regulation of the CP gene and that the gene is not responsive to copper deficiency, copper administration or copper excess in the liver.
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PMID:Hepatic ceruloplasmin gene expression is unaltered in the toxic milk mouse. 203 73

In research on congenital metabolic disorders, a biochemist can choose between the theoretical and the practical approach. The diagnosis of metabolic diseases relies on 1) the determination of the presence of metabolites under normal conditions that are direct substrates of the defective enzyme (e.g., the Gm2 ganglioside in the brain tissue of a patient with Tay-Sachs disease); 2) the determination of the lack or insufficiency of the direct product of the defective enzyme (e.g., aryl sulfatase A in the cells of patients with metachromatic leukodystrophy), hormone (hypothyroidism), or receptor (congenital hypercholesterolemia); 3) determination of substance whose reduction was established by experimentation, but the cause of the decrease is not known (ceruloplasmin in Wilson's disease); and 4) DNA analysis. Metabolic impairment of genetic origin is not treatable. The disease can be prevented by 1) removing the inappropriate metabolite (e.g., copper accumulation can be avoided by giving penicillamine or zinc salts); 2) limiting those substances in the critical phase of childhood that are components of the defective enzyme (e.g. gluten reduction in colic and protein in phenylketonuria); 3) supplementing the insufficient metabolite (e.g., phosphate in hypophosphatemia by sound for 12 hours a day); 4) protecting the patients (e.g. from light in porphyria); and 5) treatment by substances (giving coagulation factor VIII in hemophilia and thyroid hormones in hypothyroidism). There is a dilemma in subjecting patients to a diagnosis of progression to Huntington's chorea 20 years in advance or informing them about the high risk of hereditary disease for the next child (25% for the recessive and 50% for the dominant mode). Ethical committees have usually opted for a recommendation of selective abortion in clear-cut cases. Increasingly refined diagnostic methods have magnified the responsibility of the biochemist.
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PMID:[Prenatal diagnosis: a chance? risk? dilemma?]. 209 55

The study comprised 40 children of both sexes aged from 2 to 12 years, 22 suffering from bronchial asthma and 18 suffering from atopic dermatitis. Twenty healthy children of comparable age and sex to the patients were studied as controls. All the children were subjected to full history including dietetic questionnaire, thorough examination, and to estimation of serum IgE, serum ceruloplasmin, and zinc and copper levels in both serum and hairs. The mean concentrations of zinc in serum and hairs were respectively 70.3 +/- 13.2 micrograms/100 ml and 167.5 +/- 23.0 micrograms/gm in asthmatic cases and 65.9 +/- 11.7 micrograms/100 ml and 164.8 +/- 23.6 micrograms/gm in those with atopic dermatitis. These levels were significantly (p less than 0.001) decreased in comparison to the control values (88.4 +/- 11.0 micrograms/100 ml and 194.5 +/- 18.6 micrograms/gm). On the other hand, a significant (p less than 0.001) increase in serum and hairs copper was demonstrated in both allergic groups compared to the controls. Mean copper values were respectively 79.5 +/- 8.06 micrograms/100 ml and 18.7 +/- 1.9 micrograms/gm in the asthmatic cases and 81.4 +/- 8.4 micrograms/100 ml and 17.8 +/- 2.08 micrograms/gm in cases with atopic dermatitis. The control mean concentrations were 67.95 +/- 6.37 micrograms/100 ml and 14.5 +/- 2.53 micrograms/gm respectively. Significant (p less than 0.001) higher levels of serum ceruloplasmin were observed in the allergic patients compared to the controls and were correlated with the hypercupremia. The results were discussed and a good dietetic intake of high biological value protein and zinc supplement was recommended to these patients in order to correct their disturbances especially the hypozincemia which could lead to exaggeration of their allergic conditions. The field of trace elements metabolism has grown rapidly over the past few years, particularly after the development of novel techniques as the atomic absorption spectrophotometry which had allowed the reliable measurements of several trace elements in tissues and so had opened a new field for many researches (Henkin, 1976). Zinc and copper are involved in cell and tissue growth. Zinc plays an important role in DNA and protein synthesis and is intimately involved with copper as cofactors in several important enzyme systems. The effects of many pathological conditions as congestive heart failure, pneumonia, rheumatic heart diseases, bronchitis, recurrent infection, hemolytic anemia, psoriasis, and malnutrition on the levels of serum zinc, copper, and other trace elements have been of interest to investigators for a number of years (Sinha and Gabrieli, 1970; David et al., 1984).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc and copper status in children with bronchial asthma and atopic dermatitis. 213

Zinc acetate is becoming a well-established therapy for the treatment of Wilson's disease. It is excellent for maintenance therapy and for the treatment of the presymptomatic patient. Current evidence suggests that it will also be excellent for the treatment of the pregnant patient. Zinc acts by inducing intestinal cell metallothionein, which binds copper with high affinity, blocking its absorption, and causing its excretion in the stool. We have shown that zinc, even in doses as low as 25 mg daily, negatively affects copper balance. Zinc in doses of 50 mg three times daily, with all doses separated from food, controls the abnormal positive copper balance, blocks uptake of orally administered 64Cu, controls urine and plasma copper, prevents the reaccumulation of hepatic copper, and prevents the development or progression of symptoms of copper toxicosis in Wilson's disease patients. Zinc acetate will probably be licensed in the near future for the treatment of Wilson's disease. We recommend that physicians use urine and plasma copper, and urine zinc, as primary monitoring tools. In contrast to the comfortable situation with maintenance therapy, the initial treatment of acutely ill Wilson's disease patients is not well worked out. Patients with neurological disease often get worse initially on penicillamine, and zinc acts more slowly than is ideal. We have initiated studies of tetrathiomolybdate for this purpose. Studies of biliary secretions of normal subjects suggest that they excrete regulatory (excess) copper packaged in a protease-resistant ceruloplasmin fragment. This fragment is missing in Wilson's disease bile. The gene for Wilson's disease is on chromosome 13, close to the retinoblastoma locus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of zinc-copper metabolic interactions in the treatment of Wilson's disease. 225 35


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