Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 chemical plant workers producing pesticides chronic bronchitis and disturbed pulmonary ventilation are frequent. The aim of the examination of the staff (sewage-treatment plant, waste combustion plant, waste storage, industrial water pumping station)--16 males aged 21-53 years--was to assess: 1. Connective tissue metabolism--serum concentration of type I and III procollagen propeptides, collagen I telopeptide, hydroxyproline, alpha1-AP and alpha2-M antiproteases, interstitial collagenase (MMP-1) activity, as well as urine hydroxyproline and desmosine. 2. Free radical damage--serum malonic dialdehyde (TBARS) and ceruloplasmin concentration, erythrocyte antioxidant enzymes activity (SOD, catalase, GPx, GR), and neutrophils myeloperoxidase reaction. 3. Humoral (serum IgG, A and M, C3 complement component and the circulating immune complexes) and cellular (percentage of CD3, CD4 and CD8 lymphocytes) immunity rates. As compared to controls the following changes were found: 1. decreased MMP-1 activity and increased alpha2-M serum concentration; 2. increased erythrocyte SOD and GPx activities; 3. decreased percentage of T lymphocytes (CD3), increased serum concentration of the C3 complement component and the circulating immune complexes. The results were compared with those in workers of the departments producing liquid pesticides, dust pesticides and chlorfenvinphose, the changes of the investigated parameters were found to be less expressed.
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PMID:[Mechanisms of respiratory system lesions in chemical plant workers of the environmental protection department in comparison with workers of pesticide producing departments]. 1568 47

Perturbations in copper (Cu) metabolism are a characteristic of diabetes, for example, elevated plasma Cu and compromised oxidant defense related to diabetes-induced effects on Cu-containing enzymes. Herein, the redistribution of Cu in selected tissues is described in response to diabetic and nondiabetic states in rats that were fed diets adequate in (12 mg Cu/kg of diet) or deficient in (no added Cu) Cu. Diabetes was induced by intravenous administration of streptozotocin (40 mg/kg body weight). After 5 weeks, rats were gavaged with (67)Cu (0.74 MBq per rat) using the Cu-deficient diet as a vehicle (suspended 1:3 in water) and killed at various time points. The use of (67)Cu allowed for the assessment of short-term Cu distribution and its comparison to the steady-state Cu distribution, as determined by direct Cu analysis. In contrast to control rats, the adaptive mechanisms for Cu homeostasis in diabetic rats were impaired. In general, measures of Cu retention were reduced in diabetic rats compared to corresponding values for control rats. Moreover, diabetic rats had low copper, zinc superoxide dismutase activity that was reduced even further when diabetic rats were fed with low-Cu diets. However, liver and kidney metallothionein and plasma ceruloplasmin levels were elevated in diabetic rats compared to control rats. Such diabetes-related metabolic alterations were taken as measures of increased oxidative stress and inflammation, which may have implications in the progression of diabetes-related pathologies.
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PMID:Diabetes and dietary copper alter 67Cu metabolism and oxidant defense in the rat. 1586 32

The health consequences of mild copper excess in humans are unknown. In a previous study, 2 mo of supplementation with up to 6 mg Cu/L in drinking water did not induce detectable changes. Here we assessed a copper supplement at the upper level of dietary recommendations for "healthy" adults. The study was a prospective controlled trial; participants (women and men, 18-50 y old), represented the upper and lower 5% of the ceruloplasmin distribution curve obtained from a community-based sample of 800 healthy adults (n = 41/group, each approximately 50% men). Individuals received a single daily dose of 10 mg Cu for 60 d. Before and after supplementation, blood [copper, ceruloplasmin protein, homocysteine, liver aminotranferases, Cu-Zn -superoxide dismutase activity in erythrocytes (eSOD), and glutathione in peripheral mononuclear cells] and urine [copper excretion after a 5-h administration of a chelator 2,3-dimercapto-1-propano-sodium sulfonate (DMPS)] analyses were performed. After 2 mo, liver enzyme activities remained below the clinical cutoff value used to diagnose liver dysfunction, but had increased significantly in both groups and genders. These increases were no longer present 12 mo after the copper loading period was completed. Glutathione in mononuclear cells (mmol/g of protein) also increased after the 2-mo copper loading in both groups and in both genders (P = 0.01). eSOD activity, serum homocysteine concentration, and urinary copper excretion 5 h after DMPS administration were not affected. We conclude that copper administered as described induced a transient, mild, but significant elevation of aminotransferases.
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PMID:Supplementing copper at the upper level of the adult dietary recommended intake induces detectable but transient changes in healthy adults. 1617 97

An 8-year-old boy was referred to our hospital because of learning disabilities. His general cognitive functions were below the level for age, and he was diagnosed with dysphasia. The boy was transferred to a special class for children with learning problems. Three months later he was again referred to us because of acute epigastric pain. The only abnormal laboratory finding was a slightly elevated level of alanine aminotransferase. Although the symptoms disappeared in a few days, the transaminase levels remained above normal for the next 6 months. Further diagnostic work-up revealed low serum ceruloplasmin concentration and high 24-h urinary copper excretion. The hepatic copper concentration in liver biopsy was high (2900 microg/g dry weight), confirming the diagnosis of Wilson's disease. Brain MRI showed slight changes in white matter. The patient's asymptomatic sister was also diagnosed with Wilson's disease. Both siblings started penicillamine therapy and a copper-restricted diet. The copper content of the household water was found to be above average and a new plumbing system was installed. After 1 year from the initiation of the therapy, the transaminase concentrations normalized and both siblings were free of symptoms. After 2 years of therapy the patient was able to return to normal school. Wilson's disease must be borne in mind, when children are evaluated because of poor school performance, especially if they complain of abdominal symptoms.
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PMID:Poor cognitive development and abdominal pain: Wilson's disease. 1649 28

In this work, we report the X-ray crystal structure of the aerobically isolated (oxidized) and the anaerobic dithionite-reduced (at pH 8.0) forms of the native Azotobacter vinelandii bacterioferritin to 2.7 and 2.0 A resolution, respectively. Iron K-edge multiple anomalous dispersion (MAD) experiments unequivocally identified the presence of three independent iron-containing sites within the protein structure. Specifically, a dinuclear (ferroxidase) site, a b-type heme site, and the binding of a single iron atom at the four-fold molecular axis of the protein shell were observed. In addition to the novel observation of iron at the four-fold pore, these data also reveal that the oxidized form of the protein has a symmetrical ferroxidase site containing two five-coordinate iron atoms. Each iron atom is ligated by four carboxylate oxygen atoms and a single histidyl nitrogen atom. A single water molecule is found within hydrogen bonding distance of the ferroxidase site that bridges the two iron atoms on the side opposite the histidine ligands. Chemical reduction of the protein under anaerobic conditions results in an increase in the average Fe-Fe distance in the ferroxidase site from approximately 3.5 to approximately 4.0 A and the loss of one of the ligands, H130. In addition, there is significant movement of the bridging water molecule and several other amino acid side chains in the vicinity of the ferroxidase site and along the D helix to the three-fold symmetry axis. In contrast to previous work, the higher-resolution data for the dithionite-reduced structure suggest that the heme may be bound in multiple conformations. Taken together, these data allow a molecular movie of the ferroxidase gating mechanism to be developed and provide further insight into the iron uptake and/or release and mineralization mechanism of bacterioferritins in general.
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PMID:Redox-dependent structural changes in the Azotobacter vinelandii bacterioferritin: new insights into the ferroxidase and iron transport mechanism. 1658 78

We studied the effect of short-term swimming in cold water (13 degrees C) on parameters of the blood antioxidant system (activities of superoxide dismutase and catalase, concentrations of ceruloplasmin and nonprotein thiols), heme oxygenase activity, and nonprotein thiol level in mouse liver. The test parameters of antioxidant protection increased 1 h after cold exposure and remained high 1 day after treatment. These changes were accompanied by an increase in the adaptive capacity. After swimming in cold water the resistance of animals to another stress factor (administration of epinephrine) was higher compared to controls.
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PMID:Short-term cold exposure improves antioxidant status and general resistance of animals. 1692 56

This study was undertaken to examine physiological responses to acidification of environmental water in the "cobalt" variant of rainbow trout (Oncorhynchus mykiss), which exhibits malformation of the pituitary, by following changes in plasma levels of cortisol and electrolytes, blood pH, gill Na(+), K(+)-ATPase activity, and immune functions after exposure to acid water (pH 4.5). Resting levels of plasma cortisol and lysozyme were significantly lower in the cobalt variant than in the normal trout, whereas plasma ceruloplasmin was significantly higher in the cobalt variant, suggesting that some endocrine factors, lacking or deficient in the cobalt variant, are important for the regulation of its immune functions. Blood pH was slightly but significantly lower in the cobalt variant at rest. After exposure to acid water for 24 h, both the normal trout and cobalt variant showed a significant elevation in plasma cortisol, although the increased level in the cobalt variant was still lower than that in the normal trout transferred to neutral water. No differences were seen in blood pH, plasma electrolytes, and gill Na(+), K(+)-ATPase activity between the normal trout and the cobalt variant, indicating that the cobalt variant regulates ion balance when exposed to acid water, despite malformation of the pituitary. Although the normal trout showed a reduction in plasma lysozyme level after acid exposure, there was no significant change in the cobalt trout. Adverse effects of pituitary malformation on ion balance and immune functions may be compensated by extrapituitary factors in the cobalt variant when it is exposed to acid water.
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PMID:Effects of acid water exposure on plasma cortisol, ion balance, and immune functions in the "cobalt" variant of rainbow trout. 1697 89

Copper deficiency has been reported to cause a decrease in urinary taurine excretion in rats. We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats. Ten weanling male rats were assigned to either a Cu-adequate (+Cu) or Cu-deficient (-Cu) group. All rats consumed a Cu-deficient purified diet and water ad-libitum for 16 wk. The water for the (+Cu) group contained 20 mg Cu/L as CuSO(4). At wk 16, the groups differed (P < 0.05) in the following variables (means +/- SEM, -Cu vs. +Cu): body weight (BW), 375 +/- 19 vs. 418 +/- 2.9 g; food intake, 16.2 +/- 0.7 vs. 18.5 +/- 0.4 g/d; hematocrit, 0.294 +/- 0.027 vs. 0.436 +/- 0.027; hemoglobin, 95.2 +/- 9 vs 134 +/- 10 g/L; liver Cu, 8.7 +/- 2.0 vs. 65.9 +/- 2.5 nmol/g; plasma Cu, 0.38 +/- 0.09 vs. 13.4 +/- 0.61 micromol/L; plasma ceruloplasmin activity, 1.75 +/- 1.0 vs. 67.9 +/- 8.4 IU; relative heart weight, 0.56 +/- 0.04 vs. 0.35 +/- 0.02% BW; relative liver weight, 4.06 +/- 0.23 vs. 3.37 +/- 0.06% BW; and liver CSAD activity, 18.8 +/- 1.37 vs. 13.5 +/- 1.11 nmol x min(-1) x mg protein(-1). The groups did not differ at wk 16 in: plasma taurine, 249 +/- 14 vs. 298 +/- 63 micromol/L; whole blood taurine, 386 +/- 32 vs. 390 +/- 25 micromol/L; urinary taurine excretion, 82.5 +/- 15 vs. 52.0 +/- 8.3 micromol/d; liver taurine, 2.6 +/- 0.7 vs. 2.8 +/- 0.4 micromol/g; liver total glutathione, 6.9 +/- 0.48 vs. 6.3 +/- 0.40 micromol/g; liver cyst(e)ine, 96 +/- 7.1 vs. 99 +/- 5.3 nmol/g and liver CDO activity, 2.19 +/- 0.33 vs. 2.74 +/- 0.21 nmol x min(-1) x mg protein(-1). These findings support the conclusion that Cu deficiency does not affect body taurine status.
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PMID:Copper deficiency does not lead to taurine deficiency in rats. 1698 17

Fet3p is a multicopper oxidase (MCO) that functions together with the iron permease, Ftr1p, to support high-affinity Fe uptake in yeast. Fet3p is a ferroxidase that, like ceruloplasmin and hephaestin, couples the oxidation of 4 equiv of Fe(II) to the reduction of O2 to 2 H2O. The ferrous iron specificity of this subclass of MCO proteins has not been delineated by rigorous structure-function analysis. Here the crystal structure of Fet3p has been used as a template to identify the amino acid residues that confer this substrate specificity and then to quantify the contributions they make to this specific reactivity by thermodynamic and kinetic analyses. In terms of the Marcus theory of outer-sphere electron transfer, we show here that D283, E185, and D409 in Fet3p provide a Fe(II) binding site that actually favors ferric iron; this site thus reduces the reduction potential of the bound Fe(II) in comparison to that of aqueous ferrous iron, providing a thermodynamically more robust driving force for electron transfer. In addition, E185 and D409 constitute parts of the electron-transfer pathway from the bound Fe(II) to the protein's type 1 Cu(II). This electronic matrix coupling relies on H-bonds from the carboxylate OD2 atom of each residue to the NE2 NH group of the two histidine ligands at the type 1 Cu site. These two acidic residues and this H-bond network appear to distinguish a fungal ferroxidase from a fungal laccase since the specificity that Fet3p has for Fe(II) is completely lost in a Fet3pE185A/D409A mutant. Indeed, this double mutant functions kinetically better as a laccase, albeit a relatively inefficient one.
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PMID:Structural basis of the ferrous iron specificity of the yeast ferroxidase, Fet3p. 1704 92

A possible role of the macronutrients and the basic elements of carbohydrates (glucose administration or depletion), proteins (amino acids such as tryptophan and tyrosine), and fat (unsaturated fatty acids) was recently proposed for age-related changes of cognitive function, and the cognitive decline of degenerative (AD) or vascular origin. The availability and utilization of glucose has been implicated in cognitive function not only as a result of nutritional and systemic metabolic conditions, but also, although speculatively, as a crucial phase of the mechanism of action of molecules used as cognitive-enhancers. Furthermore, many lines of evidence have focused on the importance of oxidative stress mechanisms and free radical damage in AD pathogenesis. In addition, epidemiological studies have recently reported an association between alcohol and the incidence of AD and predementia syndromes. Foods with large amounts of aluminium-containing additives or aluminium from drinking water may affect the risk of developing AD, aluminium more likely acting as a cofactor somewhere in the cascade of events leading to the demented brain. A role for other metals in dementia have been speculated, given the encouraging results reported from studies on peripheral zinc concentrations, zinc supplementation, serum copper, either bound with ceruloplasmin or not, and iron metabolism in AD. Nonetheless, more data are needed to support a possible role of these metals in dementing diseases. Healthy diets, antioxidant supplements, and the prevention of nutritional deficiencies or exposure to foods and water with high content of metals could be considered the first line of defence against the development and progression of cognitive decline.
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PMID:Macronutrients, aluminium from drinking water and foods, and other metals in cognitive decline and dementia. 1711 95


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