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)

It was found in experiments on male albino rats that hypophysectomy was accompanied by an increase of potassium (on account of its accumulation in the mitochondria, nuclei and the microsomes) and copper in the liver. At the same time there was an increase in this organ of tha activity of Mg-2+-Na-+-K-+-ATPase and Mg-+-ATPase, and also a rise of ceruloplasmin activity in the blood serum. STH and TTH restored the sodium content to the normal and increased potassium level in the liver of hypophysectomized rats. ACTH and STH increased copper content in the hepatic tissue and normalized the activity of ceruloplasmin in the blood. All the hormones used promoted normalization of ATP-ase activity.
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PMID:[The effect of STH, TTH and ACTH on several aspects of copper, sodium and potassium metabolism in the livers of hypophysectomized white rats]. 16 74

A large colony of fawn-hooded (FH) rats, comprising five original families and six generations of their progeny, was developed for genetic and comparative studies of their bleeding tendency. The characteristics of the bleeding diathesis in these rats are similar to those originally reported in related rats by Tschopp and Zucker. FH rats have normal clot retraction, ADP-induced platelet aggregation and platelet ADP; variable aggregation with collagen; minimal aggregation with adrenaline and cobra venom factor; and reduced platelet ATP, ATP/ADP ratio, serotonin content and -14C-serotonin release. In comparison to age- and sex-matched Wistar rats, FH rats have significantly prolonged partial thromboplastin time, shortened Russell's viper venom time and increased factor X and XI levels. Other coagulation screening tests and specific assays for fibrinogen, plasminogen and factors VII, VIII and IX were normal. Some age- and sex-related differences in coagulation and other parameters were observed within each rat strain. Plasma proteins, glycoproteins and ceruloplasmin (copper oxidase activity) showed no abnormalities, nor did initial studies of immunoglobulins and complement. However, FH rats have significantly lower glucose and higher cholesterol levels than comparable Wistar rats.
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PMID:Characterization of the fawn-hooded rat as a model for hemostatic studies. 116 25

The introduction deals with of the history, etiology and, briefly, clinical manifestations of endemic nephropathy. The authors state that a large number of investigations have been done until today, but without producing a diagnostic test for early diagnosis of the disease. This led the authors to pursue certain laboratory investigations. The control group consisted of 30 healthy individuals while patients diagnosed as Endemic Nephropathy were grouped according to stages of the disease: initial, developed, terminal stages. Nucleotides in erythrocytes (5' UMP, 5' IMP, 5' GMP, 5,CMP, 5' AMP, 5' ADP, 5' ATP) were determined on the Acidic Aminoanalyzer, with use of a special UV detector. Catecholamines in the urine were determined by using ratiofluorometery. Creatinine phosphocinase, hydroxybutirat--dehydrogenase and 2,3 DPG were determined on the "Carlbiochem" enzymometer. LDH, its isoenzymes as well as its profile were determined by electrophoresis on starch gel. Specific proteins such as haptoglobin, alpha 2 macroglobulin, alpha 1 antitrypsin, alpha 1 acid glycoprotein, properdin factor B, ceruloplasmin were determined on the Immunochemistry Analyzer. Total cholesterol and cholesterol in lipoproteins fractions VLDL, LDL and HDL were determined on the Cholesterol Analyzer. All results were evaluated statistically. Our conclusion is that they are interesting and contribute to the diagnosis of endemic nephropathy.
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PMID:[Levels of immunoglobulins in various media from healthy pregnant women and women with diabetes mellitus and EPH gestosis]. 191 49

In situ hybridization was carried out on metaphase-prometaphase chromosomes of PGA-stimulated lymphocytes and bone marrow cells obtained from laboratory rats and mice. Plasmid cloned sequences of human apolipoprotein A-1 (Apo A-1) and ceruloplasmin (CP) cDNA fragments have been used as specific probes labelled in nick-translation reaction with 3HdTTP and 3Hd ATP. The data of our study suggest that Apo A-1 is localized in 11q14-22, 9 A2-4 and 5q36 areas in men, mice and rats, respectively. The DNA sequences of human CP cDNA most probably occupy 3q23-25, 13q24-26 and 15q13-20 areas. Heterologous in situ hybridization of other species with DNA probes does not always give reliable results in gene mapping. Thus, the data of heterologous hybridization should be considered with caution.
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PMID:[Mapping of apolipoprotein A-1 and ceruloplasmin genes on human, rat and mouse chromosomes by hybridization in situ with specific human DNA probes]. 313 94

Severe copper deficiency was induced in rats by rearing nursing dams and their offsprings on a semisynthetic diet comprising all the requisite nutrients and trace metals except copper. The copper-deprived rats exhibited growth retardation, severe anaemia, loss of caeruloplasmin, decrease of cytochrome oxidase, accumulation of salt-soluble collagen and a drastic decrease in iron in plasma and liver. Apart from these characteristic signs of deficiency, a marked inhibition of protein synthesis was found to occur both in vivo and in cell-free liver preparations. The curtailed ability to carry out endogenously coded amino acid incorporation into protein contrasted with the unimpaired poly(U)-acid-directed phenylalanine polymerization. This inhibition pattern, as well as the attendant disaggregation of the liver polyribosomes, suggested that the primary biosynthetic lesion was located at the stage of peptide-chain initiation. Concurrently with this alteration there was a pronounced depletion of the hepatic ATP content, associated with a parallel depression of mitochondrial respiration and an enhancement of ATPase activity. Supplementation of the copper-deficient diet with a 2-4-fold excess of iron (relative to the standard diet) prevented growth retardation and anaemia and restored normal energy metabolism, as well as unimpaired protein-synthesizing capacity. The conclusion that these disturbances were primarily determined by the secondary iron deficiency was also borne out by the finding that similar alterations occurred in rats maintained on a copper-sufficient but iron-deficient diet. On the other hand, the iron-fortified diet failed to reverse the other signs of copper deficiency, namely the loss of caeruloplasmin, the diminished rate of cytochrome oxidase and the increase of soluble collagen. The interrelations between the various biochemical lesions induced by deprivation of copper or iron are discussed and the possible role of ATP depletion in determining the derangement of protein synthesis is considered.
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PMID:Biochemical lesions in copper-deficient rats caused by secondary iron deficiency. Derangement of protein synthesis and impairment of energy metabolism. 625 58

Superoxide (.O-2) is demonstrated to participate at the prostaglandin phase swelling (2-4 h) of carrageenan paw edema. Superoxide production is inhibited in vitro by typical anti-inflammatory drugs, but these drugs did not scavenge superoxide which was produced by xanthine oxidase. Phosphate, pyrophosphate, ATP, ADP and sulfate were essential for superoxide production by macrophages. These anions can induce paw swelling and are reported to increase in rheumatic patients. A mixture of macrophages and lymphocytes from BCG sensitized guinea-pigs was cultured for 2 days with SOD or D-mannitol. Nitroblue tetrazolium reduction (formazan formation) was inhibited by these agents, suggesting that the hydroxyl radical (.OH) is necessary for metabolic activation of macrophage. Lympholine-like factor of which production or release is enhanced by hydroxyl radical, activates macrophage. Production of oxygen radicals may increase rapidly by this chain cycle reaction. Possible relations of oxygen radicals to prostaglandin(s) biosyntheses, chemotaxis, lysosomal enzyme release protease participation, were discussed. Endogenous SOD, epinephrine, ceruloplasmin, blood plasma proteins, inflammatory fluid, may modulate the amount of superoxide by their superoxide scavenging capacities.
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PMID:Inflammation and superoxide production by macrophages. 626 69

Microsomal lipid peroxidation induced by NADPH, but not by ascorbate, was found to be inhibited by liver cytosol. This inhibition was not dependent on glutathione and was enhanced by ADP in presence of Fe2+ at a concentration of 50 microM or higher. ATP was also effective, but not AMP or cyclic AMP. The cytosolic factor appeared to be a protein as it was heat-labile (greater than 70 degrees C), was non-dialyzable and was precipitated by ammonium sulfate and acetone. It was stable for several months in frozen state and also when heated at 50 degrees C for 10 min. The inhibition by the cytosolic protein was obtained by producing a lag in the activity of lipid peroxidation and was reversed by ceruloplasmin but not by catalase, cytochrome c, hemoglobin or superoxide dismutase. This inhibitory effect by cytosol was limited to formation of lipid peroxides whereas oxygen uptake and NADPH oxidation remained unaffected. Regulation of lipid peroxidation by nucleotide-Fe complexes and cytosolic proteins is indicated by these studies.
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PMID:Inhibition of microsomal lipid peroxidation by cytosolic protein in presence of ADP and high concentration of Fe2+. 650 75

Rats were fed copper deficient (0.9 microgram/g) or copper-supplemented diets in which the carbohydrate was either starch, sucrose, or fructose (62% by weight) for 7 wk. Regardless of the nature of the carbohydrate, copper deficiency decreased blood ceruloplasmin activity, hepatic copper and ATP levels, and increased plasma cholesterol and triglycerides. Copper deficiency in rats fed sucrose or fructose, but not those fed starch, significantly lowered blood hematocrit, Hb, and albumin and significantly increased heart and liver weight and the glucose response to a glycemic stress. Hepatic copper level was significantly lower in copper-deficient rats fed sucrose or fructose than in those fed starch. Fasting blood glucose, cholesterol, and triglyceride levels were significantly higher in copper deficient rats fed fructose than in those fed starch. During the study 14 copper-deficient rats died, one of 10 fed starch, six of 20 fed sucrose, and seven of 20 fed fructose. Death was apparently the result of rupture of the heart in the region of the apex. These results indicate that fructose-containing carbohydrates as compared to starch markedly increase the severity of copper deficiency in rats. Whether this effect is due to differences in the nature of the simple carbohydrate (fructose versus glucose) or to molecular size (simple versus complex carbohydrate) remains to be established.
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PMID:Role of dietary fructose in the enhancement of mortality and biochemical changes associated with copper deficiency in rats. 688 Oct 79

The copper-glutathione complex (Cu(I)-GSH) efficiently acted in vitro as the source of Cu(I) in the reconstitution of apoceruloplasmin. Copper was found to reinstate in the various sites in a multistep process, with metal entry into the protein in a first phase, and a second step involving conformational changes of the protein leading to the recovery of the native structural and functional properties. This latter phase was found to be strongly facilitated by Mg2+ or Ca2+ and by ATP. Both Mg2+ and ATP had to be present for optimal reconstitution. These results may shed some light on the mechanisms governing the biosynthesis of ceruloplasmin in vivo. Cu(I)-GSH was the only complex able to reconstitute ceruloplasmin at neutral pH. Glutathione may thus function to shuttle the metal from the membrane copper pump, as the Wilson disease ATPase, and ceruloplasmin in the secretory compartments of the cell. The finding that ceruloplasmin acquires the native conformation after metal entry through a complex pathway triggered by Mg2+ and ATP suggests that they may act as physiological modulators of this process in vivo.
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PMID:Reconstitution of ceruloplasmin by the Cu(I)-glutathione complex. Evidence for a role of Mg2+ and ATP. 856 46

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


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