Copper plasma level

Ceruloplasmin Binds Copper, Low Levels of This Plasma Protein Are Associated With Wilson Disease... 

Contrary to LDL, high-density lipoproteins (HDL) prevent atherosclerosis, and therefore, their plasma levels inversely correlate with the risk of developing coronary artery disease. HDL antiatherogenic activity is apparently due to the removal of cholesterol from peripheral tissues and its transport to the liver for excretion. In addition, HDL acts as antioxidants, inhibiting copper- or endothelial cell-induced LDL oxidation [180], It was found that HDL lipids are oxidized easier than LDL lipids by peroxyl radicals [181]. HDL also protects LDL by the reduction of cholesteryl ester hydroperoxides to corresponding hydroperoxides. During this process, HDL specific methionine residues in apolipoproteins AI and All are oxidized [182]. 

Zinc absorption is inhibited by most food and the elevated plasma level lasts only 5 h after a dose thus it is better given five or six times a day, 1 h before or after meals. Zinc acetate may be better tolerated than the sulfate salt. Brewer prefers 25 mg elemental zinc, administered as the acetate, five or six times a day.53 Zinc is relatively non-toxic as a drug. If more than 1 g zinc is ingested in a single dose, toxic symptoms such as abdominal pain, nausea, vomiting, fever, drowsiness and lethargy may occur. A more significant toxicity problem is zinc-induced copper deficiency which can be corrected with a supplement of 0.5 mg of copper as copper sulfate per day.53... 

Plasma levels of some hormones (thyroid and steroid hormones), vitamins (vitamin D metabolites), ions (iron, copper, and zinc) and drugs maybe low in nephrotic subjects because of the low levels of protein-bound ligands (K11), as binding proteins are lost into the urine. Ligands also may be lost in the urine together with their... 

Hypoproteinemia may result in low levels of serum calcium, ceruloplasmin, and transferrin. Because losses of iron are at most 0.5-1.0 mg/24 hr, even with the heaviest proteinuria, other factors must operate to produce iron deficiency and microcytic hypochromic anemia. Although the copper-binding protein ceruloplasmin is lost in the urine in nephrotic subjects and its plasma levels are low, plasma and red cell copper concentrations are usually normal. Zinc circulates mainly bound to albumin and also to transferrin, and thus the reported reduction zinc concentration in plasma, hair, and white cells in nephrotic patients is not surprising. 

The link between specific transition metals and various disease processes has prompted research interest into new and more effective bioanalytical methods to determine transition metals in physiological fluids. Traditionally clinical chemistry laboratories have used atomic absorption spectrophotometric (AAS) techniques to determine transition metals in physiological fluids. Although both low and high serum levels of various transition metals such as copper, iron and also zinc have been associated with various disease processes, the exact mechanisms underlying many of these conditions are still not completely understood. The following subsections describe some of the most prominent and best understood conditions associated with increased or decreased blood plasma levels of transition metals. 

Wilson s disease often involves low plasma levels of ceruloplasmin, increased plasma nonceruloplasmin copper, and increased urinary copper. The disease can involve a tenfold increase in liver copper lev els. The normal value for hepatic copper is 20 to 50 pg/g of liver dry weight). Outward signs of the disease include episodes of jaundice, vomidng, and tiredness. Bone disorders such as osteoporosis can also occur. The neurological damage includes a loss in coordination. V ilson s disease does not result in mental retardation. The rate of incorporation of copper into ceruloplasmin is reduced and biliary excretion decreases to 20 to 40% the normal rate. 

Biochemistry of Zinc and Copper Zinc in the -Cells of the Pancreas Absorption of Zinc and Copper Plasma Zinc and Copper Levels Metallothionein and Ceruloplasmin Zinc Excretion and Zinc Deficiency Copper Excretion and Copper Deficiency Genetic Diseases of Copper Metabolism Molybdenum, Sulfite, and Sulfate Molybdenum Molybdenum Biochemistry Sulfite Sulfate... 

Cp is most often measured as a screening test for Wilson s disease. Several other factors, including diet, hormone levels, and other genetic disorders, also influence plasma levels. Immunochemical assays may not distinguish between the active, copper-replete holoCp and apoCp, which is released into the circulation in most of the disorders associated with low total Cp levels. Functional assays might therefore be helpfiil in clinical circumstances, but they are more difficult to perform and less specific. 

Hosts with tumours behave similarly. They have a decreased plasma level of iron (Konaka and Matsuoka, 1967) whereas that of copper is elevated (Mortazani et aL, 1972). Some malignant tumours cause plasma zinc to fall (Davies, Musa and Dormandy, 1968), and this may be the host s doing, for many animal tumours are inhibited by a dietary deficiency of zinc (De Wys and Pories, 1972). 

The fate of ingested copper in patients with Wilson s disease may be summed up briefly as follows. Copper is absorbed from the gut and passes up the portal vein to the liver, in the early or presymptomatic stage of the illness much of the copper is trapped (see Figure 4.4). It is not used at a normal rate in the synthesis of caeruloplasmin and it is probably not excreted at a normal rate either via the bile or the intestinal wall. As the liver proteins become saturated the excess copper is only slowly cleared from the plasma compared with various control groups (see Table 4.2). The high plasma levels of non-caeruloplasmin copper permit deposition of copper at extrahepatic sites, one of which is in the kidneys (see Figure 4.5). As the illness progresses the liver looses its ability to trap copper as also do the kidneys... 

The application of the Spectroscan DC plasma emission spectrometer confirmed that for the determination of cadmium, chromium, copper, lead, nickel, and zinc in seawater the method was not sufficiently sensitive, as its detection limits just approach the levels found in seawater [731]. High concentrations of calcium and magnesium increased both the background and elemental line emission intensities. 

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