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Copper in blood

Chemists using a mass spectrometer to analyze for copper in blood plasma. [Pg.51]

Berman (B4) reported the clinical application of atomic absorption spectroscopy in the determination of copper in blood, urine, and tissues. After acid digestion of the samples, copper was complexed with EDTA and diethylthiocarbamate and extracted into a ketone. Copper levels in blood and urine from normal persons were compared to those found in patients with neurological disorders. [Pg.48]

Copper was determined with cuproine in silicate rocks, biological materials, and sea water [112,113], in environmental samples [113], steel and cast iron [114]. Neocuproine was used for determination of copper in biological materials [12,115], foods [116], sea water [117], beryllium [118], arsenic and gallium [119], tungsten [120], aluminium alloys [117], plutonium [121], tellurium [122], and fertilisers [123]. Bathocuproine was applied in determinations of copper in blood serum [124,125], water [126,127], niobium, tantalum, molybdenum, and tungsten [128], lead and nickel [129], cast iron and steel [66]. [Pg.184]

For blood analysis, the use of matrix-matched standards is an efficient strategy to compensate for the influence of viscosity, as emphasised by Rocks and co-workers, who determined zinc and copper in blood serum by flow injection flame atomic absorption spectrometry [63]. Another possibility is to exploit the standard addition method, since different viscosities can also cause a matrix effect. This approach was demonstrated by Harrow and Janata in the potentiometric evaluation of pH in blood serum [64], where the effects of sample viscosity and the presence of solid particles were successfully compensated. [Pg.163]

Spectrophotometric determination of the protein ceruloplasmin in blood serum. The determination of this protein has replaced the determination of copper in blood serum. [Pg.732]

It has been suggested that in some forms of the disease there may be an elevated sequestration of caeruloplasmin by the parenchymal cells of the liver, leading to a low level of this glycoprotein in serum and a heavy load of copper on the liver. Copper in blood will increasingly come to bind to those proteins for which it has a lower affinity than for caeruloplasmin. Some copper reaches the brain, for which it is intensely toxic. [Pg.294]

The average concentration of copper in blood is 1.10 mg/1 in men and 1.23 mg/I in women. More than 90% of copper in the body is found in the blood plasma. The major copper-binding substance in blood plasma is monomeric glycometaUoprotein ceruloplasmin from a group of a2-globulins (132 kDa), which is composed of 1046 amino acids and contains about 7-8% of sugar components. Ceruloplasmin has a blue colour and in the normal state one molecule of ceruloplasmin contains six atoms of copper (at full saturation additional binding sites may be occupied by an additional two copper atoms). Blood plasma contains about 300 mg/1 of ceruloplasmin. In erythrocytes, copper occurs in another protein called erythrocuprein (31 kDa) and in the enzyme superoxide dismutase. [Pg.438]

Copper. AH human tissues contain copper. The highest amounts are found in the Hver, brain, heart, and kidney (102). In blood, plasma and erythrocytes contain almost equal amounts of copper, ie, ca 110 and 115 mg/100 mL, respectively. [Pg.385]

Nicdermeier, W. (1965). Concentration and chemical state of copper in synovial fluid and blood serum of patients with rheumatoid arthritis. Ann. Rheum. Dis. 24, 544-548. [Pg.111]

Mechanisms by which copper deficiency results in neutropenia, with emphasis on the process of cellular differentiation and the viability of neutrophils in blood and marrow (Percival 1995)... [Pg.209]

Increase in blood and urine Mo levels, increases in serum ceruloplasmin, increased xanthine oxidase activity (11) Increased uric acid, decreased copper excretion, high incidence of gout-like disease (11)... [Pg.1566]

Other workers have determined zinc in serum by direct dilution 87> 88). McPherson and George 89) determined total copper and zinc of red cells and the free copper and zinc of plasma and dialysis fluids of patients undergoing regular hemodialysis, using atomic absorption spectroscopy. Spry and Piper 90) determined zinc in whole blood and plasma in blood cells of iron deficient rats. The zinc concentrations were raised in the iron deficient rats. [Pg.90]

In 1847 E. Harless discovered the presence of copper in the blood of the octopus Eledone and the snail Helix pomatia (172, 173). Investigation of the phenomenon by which the blood and tissues of certain marine animals turn blue on exposure to air finally led to the discovery that the blood plasma of such animals contains copper combined with a protein. Because of its analogy to hemoglobin and its ability to carry oxygen, L. Fredericq in 1878 named the copper-containing protein in the blood of Octopus vulgaris hemocyanin (173, 174). [Pg.29]


See other pages where Copper in blood is mentioned: [Pg.253]    [Pg.6]    [Pg.56]    [Pg.360]    [Pg.304]    [Pg.313]    [Pg.314]    [Pg.1328]    [Pg.1329]    [Pg.667]    [Pg.426]    [Pg.435]    [Pg.253]    [Pg.6]    [Pg.56]    [Pg.360]    [Pg.304]    [Pg.313]    [Pg.314]    [Pg.1328]    [Pg.1329]    [Pg.667]    [Pg.426]    [Pg.435]    [Pg.329]    [Pg.185]    [Pg.212]    [Pg.263]    [Pg.588]    [Pg.275]    [Pg.106]    [Pg.326]    [Pg.152]    [Pg.426]    [Pg.676]    [Pg.133]    [Pg.134]    [Pg.135]    [Pg.136]    [Pg.188]    [Pg.195]    [Pg.198]    [Pg.203]    [Pg.1547]    [Pg.43]    [Pg.342]    [Pg.184]    [Pg.309]    [Pg.120]   


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Blood copper

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