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. The effect of acute duodenal infusion of 99Mo-labelled sodium tetrathiomolybdate on caeruloplasmin (ferroxidase; EC 1.16.3.1) was examined in sheep. The diamine oxidase activity of this enzyme with respect to two substrates, p-phenylenediamine and o-dianisidine (both at their apparent Km concentrations) was inhibited. 2. The 99Mo appeared rapidly in plasma and was at first present predominantly in a trichloroacetic acid insoluble form; inhibition of oxidase activity was related to the levels of TCA-insoluble Mo. The behaviour of the copper prosthetic groups of caeruloplasmin was altered since some plasma Cu precipitated with the protein fraction after TCA treatment. The appearance of TCA insoluble Cu was related to the level of TCA-insoluble 99Mo and corresponded to the inhibition of diamine oxidase activity.
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PMID:The fate of 99Mo-labelled sodium tetrathiomolybdate after duodenal administration in sheep: the effect on caeruloplasmin (EC 1.16.3.1) diamine oxidase activity and plasma copper. 677 44

The present study describes the effect of fluoride (10 mg NaF/kg body weight/day) on the total protein-bound sialic acid and ceruloplasmin levels in rabbit serum after receiving sodium fluoride intragastrically for 3, 5, 8 and 10 months. The total protein-bound sialic acid and ceruloplasmin levels in serum were reduced, whereas the fluoride levels were increased showing a cumulative effect. It is suggested that the decreased circulatory sialic acid and ceruloplasmin levels with increased serum fluoride may be used in an early detection of fluorosis.
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PMID:Serum sialic acid and ceruloplasmin levels in experimental fluorosis. 683 84

A simple method is described for the analysis of proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis combined with crossed immunoelectrophoresis. The technique allows the identification of specific proteins and estimation of their molecular weights after the electrophoresis of complex mixtures such as blood plasma. Human ceruloplasmin was estimated to have a molecular weight of 128,000 using this method. Reduction of plasma with 2-mercaptoethanol in the presence of protease inhibitors did not result in dissociation of ceruloplasmin into detectable smaller subunits, suggesting that native ceruloplasmin is composed of a single polypeptide chain.
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PMID:Evidence for a single-chain structure of native human ceruloplasmin using sodium dodecyl sulfate-polyacrylamide-crossed immunoelectrophoresis. 684 8

Serum copper and zinc levels were measured in 84 treated male epileptics, aged between 6 and 18 years, by an atomic absorption spectroscopic method. These patients were selected randomly from a residential special school. Twenty drug-free healthy but educationally subnormal (ESN) male subjects of similar age group from the same school acted as controls. No abnormality in serum zinc level was observed. In nineteen (22.6%) epileptics, copper levels were above the upper level of normal range (20.5 mumol/l), whereas this was only marginally elevated (20.8 mumol/l) in one (5%) ESN subject. The mean copper level in all epileptics was higher than the controls (P less than 0.01), but there was no difference between the epileptics treated with sodium valproate alone and the ESN group. The patients who were receiving carbamazepine either as monotherapy or in combination with other drugs except phenytoin, had higher mean copper levels than the controls (P less than 0.01). A similar observation was made in relation with phenytoin polytherapy (but excluding carbamazepine). There also appeared to be an association between the high serum copper levels and diffuse/generalized electroencephalographic changes (P less than 0.001). Some antiepileptic drugs, particularly carbamazepine, can produce such electroencephalographic abnormalities. It is concluded that hypercupraemia observed in these treated epileptics were related to the induction of caeruloplasmin synthesis by phenytoin and carbamazepine.
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PMID:Hypercupraemia induced by antiepileptic drugs. 688 97

Highly purified ceruloplasmin mRNA was isolated from rat liver polyribosomes. The molecular weight of ceruloplasmin mRNA is in a range from 1.05 to 1.25 . 10(6) daltons which is large enough to code for a putative precursor of ceruloplasmin (approximately 700 amino acid acids). Ceruloplasmin mRNA contains 3'-terminal poly(A) the length of which varies from 38 to 165 nucleotides. The 5'-end of ceruloplasmin mRNA is blocked with confronting m7G residue which is a component of cap I (m7G5'ppp5'XmpAp). The addition of ceruloplasmin mRNA to wheat-germ cell free system programmed the synthesis of a product that was largely precipitated by anti-ceruloplasmin immunoglobulins. The translation product was homogeneous in polyacrylamide gel-sodium dodecylsulfate electrophoresis. Cell-free translation of ceruloplasmin mRNA was sensitive to inhibition by cap analogue.
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PMID:Highly purified ceruloplasmin messenger RNA from rat liver. Physico-chemical and functional characteristics. 724 26

Functional roles of peroxynitrite in N-methyl-D-aspartate (NMDA)- and sodium nitroprusside (SNP)-evoked releases of acetylcholine (ACh) from cerebral cortical neurons in primary culture have been investigated. NMDA increased the release of ACh in a dose-dependent manner, which was significantly suppressed by (+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cycloheptan-5,10-imine (MK-801), a non-competitive antagonist specific for the NMDA receptor complex, and NO synthase inhibitors. SNP also showed a concentration-dependent increase in ACh release. Hemoglobin significantly abolished the stimulatory effects of both NMDA and SNP on ACh release. In addition, superoxide anion scavengers such as superoxide dismutase and ceruloplasmin significantly reduced the increased ACh release evoked by NMDA and SNP. Synthesized peroxynitrite dose-dependently elevated the release of ACh. These results indicate that the increased release of ACh by NMDA and SNP is mediated through peroxynitrite formed in the reaction of superoxide anion with nitric oxide produced by NMDA receptor activation and liberated from SNP rather than nitric oxide itself.
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PMID:Involvement of peroxynitrite in N-methyl-D-aspartate- and sodium nitroprusside-induced release of acetylcholine from mouse cerebral cortical neurons. 747 28

The role of sodium molybdate (1 mg/kg, intraperitoneally, once daily) supplementation during the course of lead exposure (0.1% lead acetate in drinking water for 4 weeks) in preventing the accumulation of lead in blood and soft tissues and in restoring altered lead-sensitive biochemical variables and the levels of hepatic glutathione, lipid peroxidation, blood Na, blood K, and serum ceruloplasmin was investigated in rats. The data indicate that sodium molybdate significantly protected the uptake of lead in blood, liver, and kidneys and restored the lead-induced inhibited activity of blood delta-aminolevulinic acid dehydratase, elevation of blood zinc protoporphyrin, hepatic lipid peroxidation, and serum ceruloplasmin. The results suggest a significant role of sodium molybdate in preventing plumbism.
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PMID:Preventive effects of sodium molybdate in lead intoxication in rats. 750 10

Acute inflammation was induced in pigs using a single subcutaneous turpentine injection. The acute phase serum protein response was analyzed using crossed immunoelectrophoresis and immunodiffusion. The concentration of C reactive protein and haptoglobin increases 5-7 times 48 h after the injection, whereas the concentration of an alpha 2-globulin, named pig major acute phase protein (pig-MAP), increases at least 15-fold. A molecular mass of 115 kDa for pig-MAP was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. This protein did not crossreact with antisera to human hemopexin, ceruloplasmin, H-kininogen and complement factor C3. Albumin and alpha-lipoprotein were negative acute phase proteins because their concentration significantly decreased during inflammation. Finally, the concentration of alpha 1-acid glycoprotein, fetuin, alpha 1-protease inhibitor, transferrin and alpha 2-macroglobulins, as well as total proteins, did not change significantly during inflammation.
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PMID:Characterization of the acute phase serum protein response in pigs. 752 7

Our aims were to analyze the protein composition of the organic matrix of urinary stones and to investigate the role of albumin in its constitution. Five different morphological types of stones were studied. Proteins extracted from the stone were submitted to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed by immunoblotting with antibodies to 13 urinary proteins. Nine of the 13 proteins were found in all types of stone: human serum albumin (HSA), alpha 1-acid glycoprotein (alpha 1-GP), alpha 1-microglobulin (alpha 1-M), immunoglobulins (Igs), apolipoprotein A1 (apo-A1), transferrin (Tr), alpha 1-antitrypsin (alpha 1-T), retinol-binding protein (RBP) and renal lithostathine (RL). The beta 2-microglobulin (beta 2-M) was present only in calcium oxalate and uric acid stones. In contrast, ceruloplasmin, haptoglobin and Tamm-Horsfall protein (THP) were detected in none of them. Because HSA appeared as the major protein component in all stones, we wondered whether it might play a specific role in the constitution of the stone matrix. Association of HSA with urinary proteins that were present in stones was demonstrated by showing that proteins present in the matrix comigrated with HSA on gel filtration, whereas proteins that were absent did not. Moreover, HSA induced the binding of stone matrix proteins to an albumin-specific affinity column. Finally, we evidenced HSA binding to calcium oxalate monohydrate (COM) crystals in a solution similar to urine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of the soluble organic matrix of five morphologically different kidney stones. Evidence for a specific role of albumin in the constitution of the stone protein matrix. 761 35

The functional significance of peroxynitrite in the release of [3H]GABA induced by nitric oxide (NO) liberated from NO generators was investigated using cerebral cortical neurons in primary culture. NO generators such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) increased [3H] GABA release in a dose-dependent manner. These increases in [3H]-GABA release were significantly inhibited by hemoglobin, indicating that those NO generators evoke the release of [3H] GABA by the formation of NO. Two types of superoxide scavengers, Cu2+/Zn2+ superoxide dismutase and ceruloplasmin, significantly reduced the increase in [3H]-GABA release induced by both SNP and SNAP, which assumes that NO requires superoxide to induce [3H]-GABA release from the neurons. In addition, synthesized peroxynitrite induced a dose-dependent increase in [3H]-GABA release from the neurons. These results indicate that NO-induced [3H] GABA release is mediated by peroxynitrite formed by the reaction of NO with superoxide.
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PMID:Nitric oxide-induced [3H] GABA release from cerebral cortical neurons is mediated by peroxynitrite. 764 88


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