Serum copper

Evenson, M. A. and Warren, B. L. "Determination of Serum Copper by Atomic Absorption, With Use of the Graphite Cuvette". Clin. Chem. (1975), 21, 619-625. 

Blake, 1989 Winyard et al., 1989). We suggest that within the inflamed rheumatoid joint (or the artery wall in atherogenesis), the production of ROM and proteases by endothelial cells and/or macrophages may cause the release of copper ions from Cp (see Section 2.2.3.2). It has been reported that Cp is cleaved faster in serum from patients with inflammatory diseases when compared to normal serum (Laurell, 1985). The oxidative modification of LDL by Cp-derived copper ions may explain the observation that increased serum cholesterol values are associated with accelerated atherosclerotic progression in men with high serum copper concentrations (Salonen et al., 1991). 

In addition, treatment with zinc acetate helps to reduce serum copper levels. Zinc acetate is a relatively nontoxic agent which blocks intestinal copper uptake and induces... 

Weanling foals, age 3 months, fed diets containing 7.7 mg copper/kg plus 29, 250,1000,or2000mgZn/kg ration for 15 weeks. At start, serum zinc level was 0.6 mg/L and serum copper level 1.4 mg/L... 

Foals fed 29 or 250 mg Zn/kg diets had normal serum copper and zinc concentrations. Those fed 1000 or 2000 mg Zn/kg diet became hypocupremic in 5 to 6 weeks and developed lameness owing to cartilaginous disease similar to osteochondritis dessicous. Foals fed high zinc diets became lame when serum copper fell to 0.3 mg/L for >1 week at end of study arthritic foals had <0.2 mg copper/L serum. Serum zinc concentrations rose to >2 mg/L within 2 weeks at 1000 or 2000 mg Zn/kg diet liver zinc was <333 mg/kg DW at diets of <250 mg Zn/kg, 2728-3511 mg/kg DW at 1000 mg Zn/kg diet, and 4364-4524 mg/kg DW at the highest dietary loading of 2000 mg Zn/kg in 15 weeks Decreased growth, lameness, bone deformities, death. 

For other trace elements, about which relatively less is known, the evidence for substantial variability is on the whole less impressive though by no means nonexistent. With respect to copper, Valleel4 says that "most investigators agree that the serum copper level of normal individuals is remarkably constant, and in our experience, in... 

Bert L. Vallee, "The Time Course of Serum Copper Concentrations of Individuals with Myocardial Infarctions. I," mimeographed paper, undated, p. 1. 

A 6-month-old infant is seen in the emei ency room with a fractured rib and subdural hematoma. The child s hair is thin, colorless, and tangled. His serum copper level is 5.5 nM (normal for age, 11-12 nM). Developmental delay is prominent. A deficiency of vhich enzyme activity most dosely relates to these symptoms ... 

Increase the daily dose only when the clinical response is not adeguate or the concentration of free serum copper is persistently above 20 mcg/dL. Determine optimal long-term maintenance dosage at 6- to 12-month intervals. 

In the preceding iron determination, the results would be about 10% high because serum copper also forms a colored complex with ferrozine. Interference is eliminated if neocuproine or thiourea is added. These reagents mask Cu+ by forming strong complexes that prevent Cu+ from reacting with ferrozine. 

Serum copper concentrations have been shown to increase in active cancer and decrease in remission thus it seems likely that some copper-dependent process is required for response or remission. A number of copper complexes have been tested and found to have rodent antitumor activity. There appear to be copper complexes which serve in a homeostatic fashion to prevent development of neoplasms. If this physiologic response fails at some point, tumors may be allowed to grow. 

Heinemann G. [Plasma iron, serum copper, and serum zinc during therapy with ovulation inhibitors.JMed Klin 1974 69(20) 892-6. 

Sex hormones can cause changes in metal metabolism, including both increased and reduced plasma zinc concentrations and raised serum copper however, serum magnesium is not affected (191). The clinical importance of these effects is not known. 

Holmberg, C. G. and C. B. Laurell Investigation in serum copper. I. Nature of serum copper and its relation to the iron-binding proteins in human serum. Acta. Chem. Scand. 1, 944 (1947). 

A 6-month-old infant has been fed unmodified cow s milk supplemented with com flour. He was healthy except that he was severely anemic, and an X-ray of his wrist showed retarded bone development. His hemoglobin was only 4.5 g/dL, and he had an elevated serum alkaline phosphatase. He was treated with iron supplements, folate, and ascorbic acid to no avail. Then serum copper analysis was done, and it showed a level of 9 fig/dL (normal is 85-163 /ig/dL). Thereupon his diet was supplemented with copper sulfate, and he showed dramatic improvement. Address the following questions ... 

A. J., Cai, D. Y., and Klinman, J. P., 1994, Primary structures for a mammalian cellular and serum copper amine oxidase, J. Biol. Chem., 269 9926n9932. 

Serum copper levels (Serum copper levels... 

The disease is a rare inherited disorder characterized by a progressive degeneration of the lenticular nucleus in the brain and by cirrhosis of the liver. Barbeau et al. (Bl) studied a case of Wilson s disease which presented normal ceruloplasmin and serum copper values but increased excretion of kynurenine, 3-hydroxykynurenine, and conjugated anthra-nilic acid in xurine after an oral dose of 2 g L-tryptophan. This defect in tryptophan metabolism could be related to that of other amino acids and to the actual content of ceruloplasmin in Wilson s disease (Bl). These findings corroborated Marver s (M2) investigations demonstrating a definite excretion of kynurenine and 3-hydroxykynurenine in abnormal proportions after a tryptophan load in a case of Wilson s disease. 

Elevation of serum copper is found in cholestasis, obstructive jaundice, primary biliary cholangitis, malignant tumours, kwashiorkor, exocrine pancreatic insufficiency, during the last trimenon of pregnancy and after administration of oestrogens. A decrease in serum copper is typical of Wilson s disease. In some rare cases, it is caused by familial benign hypocupraemia and nutritional deficiency in neonates. 

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