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)

1. Copper deficiency was induced in five Friesian cattle offered a semi-synthetic diet containing less than 1 mgCu/kg. Changes in blood and liver Cu contents and in the Cu-containing enzymes, ferroxidase I (caeruloplasmin; EC 1.16.3.1) and monoamine oxidase (EC 1.4.3.4) of plasma and cytochrome oxidase (EC 1.9.3.1) of liver and skeletal muscle were monitored during Cu depletion. 2. Rapid decreases in blood and liver Cu and plasma ferroxidase I activity were found at least 80 d before the first appearance of overt clinical signs of deficiency. Plasma monoamine oxidase and liver cytochrome oxidase activities decreased less rapidly and thus may provide useful indices of chronic Cu depletion.
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PMID:Biochemical and pathological changes in tissues of Friesian cattle during the experimental induction of copper deficiency. 17 48

Following extensive bowel resection, a young woman experienced severe malnutrition; subsequent administration of parenteral nutrition precipitated the copper deficiency syndrome. This consisted of hypocupremia, subnormal ceruloplasmin levels, anemia, and severe neutropenia. The bone marrow was megaloblastic, vacuolated, and sideroblastic; granulocytic maturation was not observed beyond the myelocyte stage. Copper sulfate therapy was followed by a marked reticulocytosis, increase in hematocrit, and recovery of neutrophils. Additional studies indicated that both serum and urinary erythropoietin values were low; serum activity increased after copper supplementation. Abnormal granulopoiesis was demonstrated using the in vitro granulocyte colony assay. The patient's granulcoytic stem cells were normal on two occasions; however, mixing studies showed that culture of the patient's copper-deficient marrow with her copper-deficient serum yielded significantly reduced numbers of granulocyte colonies. Thus, copper appears to be a necessary element for normal hematopoiesis; lack of this trace element may result in ineffective erythropoiesis and granulopoiesis.
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PMID:Observations on the anemia and neutropenia of human copper deficiency. 30 69

Weekly determinations of serum copper (Cu) and zinc (Zn) were made in eight adult patients receiving total parenteral nutrition (TPN) for 3 to 13 weeks. Serum Cu decreased in all eight patients. Five of eight patients had hypocupremia lasting at least 2 consecutive weeks and three of the five had Cu levels of 30 mug/dl or lower. Low levels of serum ceruloplasmin provided supportive evidence of Cu deficiency in the three patients with the lowest Cu levels. Two patients who had Cu less than or equal to 20 mug/dl demonstrated declines in hemoglobin which were probably due to Cu deficiency. The mean rate of decline in serum Cu was 10.8 mug/dl/week. After resumption of oral feedings in five patients, the mean rate of increase in Cu was 14 mug/dl/week. The sharpest rise in Cu was seen during the 2nd week after oral feedings were resumed in four of the five patients. Three of eight patients had serum Zn levels less than 70 mug/dl for at least 2 consecutive weeks. Serum Zn decreased at a mean rate of 6.6 mug/dl/week. There was a further decline in serum Zn in three of five patients in whom measurements were made after resumption of oral intake. Concentrations of Zn in TPN solutions varied between 0.63 and 1.0 mg/liter. Cu was undetectable in TPN solutions.
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PMID:A prospective study of serum copper and zinc levels in patients receiving total parenteral nutrition. 81 16

To examine the mechanisms of holo-caeruloplasmin biosynthesis, we measured the serum caeruloplasmin concentration and oxidase activity, hepatic caeruloplasmin mRNA content and hepatocyte caeruloplasmin biosynthesis and secretion in normal and copper-deficient rats. Copper deficiency resulted in a near-complete loss of serum caeruloplasmin oxidase activity, yet only a 60% reduction in serum caeruloplasmin concentration and no change in the abundance of hepatic caeruloplasmin mRNA or the rate of caeruloplasmin biosynthesis. Both interleukin-1 alpha and lipopolysaccharide increased hepatic caeruloplasmin mRNA content and caeruloplasmin biosynthesis in normal and copper-deficient animals, but neither mediator increased caeruloplasmin oxidase activity in the copper-deficient group. Pulse-chase studies in primary hepatocytes from normal and copper-deficient rats revealed that the secretory rates for newly synthesized caeruloplasmin were identical, despite little or no holo-caeruloplasmin synthesis in hepatocytes of copper-deficient rats. We conclude that hepatocyte copper content has no effect on hepatic caeruloplasmin-gene expression or caeruloplasmin biosynthesis and that the incorporation of copper into newly synthesized caeruloplasmin is not a rate-limiting step in the biosynthesis or secretion of the apoprotein from rat hepatocytes.
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PMID:Mechanisms of caeruloplasmin biosynthesis in normal and copper-deficient rats. 155 68

The purpose of this study was to determine what levels of starch or glucose replacement for fructose in the copper-deficient diet (copper) can minimize the fructose-copper interaction. Experimental diets contained either 100% fructose as the carbohydrate source, or the fructose was partially replaced with 50% starch, 50% glucose, 75% starch, or 75% glucose. Diets were either copper adequate (7-8 ppm) or inadequate (less than 1 ppm). Male weanling rats were fed their respective diet for 5 weeks and then fasted overnight. After decapitation, blood was collected and liver and heart were removed. Plasma copper was significantly reduced and ceruloplasmin was not detected in all copper-deficient groups. Copper deficiency increased plasma cholesterol, as well as heart and liver weight in the glucose groups, but not in the starch groups. Those organ weights were heavier in glucose-copper than starch-copper rats. Erythrocyte copper-zinc-superoxide dismutase activity was greater in starch-copper rats. Erythrocyte copper-zinc-superoxide dismutase activity was greater in starch-copper than glucose-copper rats regardless of carbohydrate amount. Hepatic copper concentration of the group fed starch-copper was twice levels observed in glucose-copper. The 50% glucose rats had lower hepatic copper than the 75% glucose rats. Hepatic copper-zinc-superoxide dismutase activity showed patterns similar to hepatic copper. Cardiac copper was greater in starch-copper than glucose-copper rats. Cardiac copper-zinc-superoxide dismutase activity was equally reduced in all copper-deficient groups. The 50% starch-replaced diet was more effective in minimizing copper deficiency than the 75% glucose-replaced diet. This poorer improvement of copper deficiency by glucose than starch may partially be due to a more severe reduction of food intake in glucose than in starch diets.
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PMID:Comparison of copper status in rats when dietary fructose is replaced by either cornstarch or glucose. 234 47

Copper deficiency developed in a five-month-old prematurely born infant with an abdominal wall closure defect and a small bowel fistula under long-term parenteral nutrition. The first manifestations were typical bone changes including diffuse osteoporosis, delayed bone age, widened cupped metaphyses with beaks and a fracture, subperiosteal hematomas and ossifications in the shafts of long bones, and a diaphyseal fracture. Other findings that confirmed the diagnosis included edema of the limbs with pseudoparalysis, neurologic abnormalities, anemia, leukoneutropenia, and very low serum levels of copper and ceruloplasmin. Following initiation of copper supplementation, clinical, hematological and biological disorders resolved within a few days and roentgenologic bone abnormalities within four months. Copper deficiency develops only in the presence of specific risk factors, that are often combined in a single patient: inadequate stores due to prematurity, excessive loss due to chronic diarrhea, exudative enteropathy, a proximal stoma, or a biliodigestive fistula; and inadequate intake due to malabsorption or long-term exclusive parenteral nutrition (EPN). Appropriate copper supplementation is needed in all these high risk situations. Early, continuous copper supplementation is required for young children under EPN. Serum copper assays should be included among the periodically monitored biochemical parameters.
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PMID:[Nutritional copper deficiency. Apropos of a case]. 250 Aug 84

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

Anemia and neutropenia developed in a man who took pharmacologic doses of supplemental zinc. Laboratory investigation showed high zinc level, hypocupremia, low ceruloplasmin level, and ringed sideroblasts. All resolved after withdrawal of zinc. Self-administered zinc appears to have caused severe copper deficiency, with secondary anemia and neutropenia. Physicians should be aware of this deleterious and completely reversible effect of megadose mineral therapy. Zinc ingestion or exposure should be considered in the differential diagnosis of unexplained anemia, leukopenia, or sideroblastic anemia.
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PMID:Copper deficiency and sideroblastic anemia associated with zinc ingestion. 340 36

Conflicting reports regarding copper status in thermal injury patients have been published. We determined serial serum-copper and serum-ceruloplasmin levels and 24-h urinary excretion of copper in 23 patients with second- and third-degree thermal burns. Throughout hospitalization, mean serum-copper concentration was significantly depressed; lowest levels were found in patients with greater than 40% total body surface area burns. Serum ceruloplasmin was also depressed, an unexpected finding because this protein is a positive acute-phase reactant poststress. Mean urinary excretion of copper was elevated, reaching 2.5 times the upper limit of normal 2 wk postburn. Depressed serum-copper levels paralleled the serum-ceruloplasmin levels rather than the increased urinary-copper losses. Further studies are required to determine the mechanism(s) of this altered copper metabolism and whether physiological or biochemical evidence of copper deficiency accompanies the observed hypocupremia.
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PMID:Serum copper and ceruloplasmin levels and urinary copper excretion in thermal injury. 378 37

To investigate the hypothesis that copper deficiency in the rat could result in increased susceptibility to CCl4-induced lipid peroxidation caused by decreased free radical defenses, we performed a series of experiments administering CCl4 to copper-deficient and control rats. Peroxidation after CCl4 administration was monitored by measuring the evolution of expired ethane in closed metabolic chambers. Rats were fed one of two copper-deficient diets based on either evaporated milk or powdered milk. Compared with control values, liver copper content, liver superoxide dismutase activity, and plasma ceruloplasmin level were significantly decreased in copper-deficient rats fed either of the diets. Liver glutathione peroxidase activity was also decreased in the copper-deficient rats fed the evaporated milk diet. Ethane evolution was markedly increased in both copper-deficient groups as compared with their controls. Copper deficiency was also found to produce increases in hepatic iron concentrations, but normal rats loaded with iron dextran to increase hepatic iron concentrations into a range similar to that found in the copper-deficient rats did not exhibit increased ethane evolution after CCl4 administration. Copper deficiency in the rat results in increased CCl4-induced lipid peroxidation.
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PMID:Effects of copper deficiency on carbon tetrachloride-induced lipid peroxidation. 380 65


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