Blood copper

Biological Roles of Zinc and Copper. Zinc and copper are essential cofactors at the active site of a number of enzymes. Zinc is a component of more than 200 proteins and enzymes (Table II). Copper, sim-lleT to iron, participates both in redox reactions and as a proton doner (Table III). The normal human adult body contains approximately 50-100 mg of copper and 2.0 g of zinc. The vast majority of tissue copper is found in the liver, kidney, heart and brain. In the blood, copper exists within the red blood cell as superoxide dlsmutase and in the serum as ceruloplasmin. Copper is a component of aerobic metabolism, bone synthesis, and erythrocyte development. Zinc is found primarily in the liver, kidney, bone and prostate. Zinc is essential for normal growth of tissues, wound repair, skin structure, reproduction, taste perception, and the prevention of dwarfism. 

A13. Axtrup, S., The Blood Copper in Anaemias of Children with Special Reference to Premature Cases. P. H. Lunstedt Univ. Bokhandel, Lund, 1946. 

Biological systems, picosecond spectroscopy, 201-20 Blood, copper and zinc analyses, 112 Blooming... 

These changes in serum copper were found not to be related to sex but were most pronounced in the fever phase and correlated with a decrease in haemoglobin and an increase in ESR [45]. Non-sex-related alterations of copper were confirmed by Van Ravesteijn, who also found that RBC copper decreased in spite of an increase in whole blood copper [49]. 

Epileptic patients also have elevated blood copper concentrations [302-304]. As shown in Table 6.1, the brain contains more copper than any other nonstorage tissue in the human body [2], and brain tissues are known to require copper-dependent enzymes listed in Table 6.2 for normal development and function [ 1,8,135]. In addition, it has been pointed out that copper-dependent processes are required for modulation of prostaglandin syntheses [135], lysosomal membrane stability [135], and the activity of histamine (see previous Section on gastrointestinal ulcers), which are also important for normal brain functions. 

Mycoplasmal infection may also play a role in the etiology of rheumatoid diseases [556,557]. Since copper complexes of 1,10-phenanthroline, 2,9-dime-thyl-l,10-phenanthroline, 1,3-disubstituted isoquinolines, and 2,2 -bipyridine have been shown to be effective antimycoplasmal agents [558-561], this approach to understanding the effectiveness of therapy and the physiological response associated with elevated blood copper levels in arthritic diseases also merits study. 

In dogs exposed to high levels of dietary copper, high blood copper levels were observed leading to the increased urinary excretion of both copper and co-present cadmium (Kodama 1988). 

During the early stages of WD the liver is capable of storing 30 to 50 times more copper than normal, with no overt clinical disorder. When large amounts of copper are ultimately released from the liver into the bloodstream - as in the case of massive necrosis of liver parenchyma - a severe hemolytic anemia may ensue (Erslev 1986). The release of copper into the bloodstream is usually more gradual and, over the years, plasma concentrations of free copper may rise from little more than zero to 25 to 50 pg 100 mD or more. The increased levels of blood copper cannot be excreted due to biliary excretion failure, and so the copper will slowly accumulate in the various compartments of the body, especially the lenticular nucleus of the brain. If untreated, WD is ultimately fatal. 

Dick AT (1954) Preliminary observations on the effect of high intakes of molybdenum and inorganic sulphate on blood copper and fleece character in crossbred sheep. Aust Vet J 30 196-206. 

A. Specific levels. If copper salt ingestion is suspected, a semm copper level should be obtained. Normal serum copper concentrations average 1 mg/L, and this doubles during pregnancy. Semm copper levels above 5 mg/L are considered very toxic. Whole-blood copper levels may correlate better with acute intoxication because acute excess copper is carried in the red blood cells however, whole-blood copper levels are not as widely available. 

Blood copper levels were significantly (P <0.01) elevated in 11 out of 13 patients with asbestosis (Avolio et al. 1988). 

In blood, copper is found in both red cells and plasma. Copper of the red cells is tightly bound to a colorless protein (mol wt approximately 33,000) containing 2 atoms of copper per molecule (erythrocu-prein). Erythrocuprein has an isoelectric point of 5.3 and presents no oxidative properties. Its function in the physiology of the cell is not clear, although there is a rapid exchange between the red cell copper and the plasma copper [47]. 

The normal range of concentration of copper in the blood of healthy animals is wide but very similar in all mammalian species studied (see Table 3). Not only are there considerable variations from individual to individual, but the same animal is subject to significant diurnal and day-to-day fluctuations for no known reasons. These normal levels are, however, markedly reduced by a low copper diet. Subnormal blood copper concentrations have been demonstrated in rats and pigs suffering from experi-... 

A deficiency in blood copper, which may Ere caused by urinary loss of cerulopitismin (the copper binding protein of the plasma) in nephrosis (degeneration of the kidneys) or by mal-aErsorption of copper in sprue. 

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