Copper supplements

Plant and Animal Nutrient. Copper is one of seven micronutrients that has been identified as essential to the proper growth of plants (87). Cereal crops are by far the most affected by copper deficiency (see Wheat and other cereal grains). Greenhouse studies have shown yield increases from 38% to over 500% for wheat, barley, and oats (88) using copper supplementation. A tenfold increase in the yield of oats was reported in France (89). Symptoms of copper deficiency vary depending on species, but often it is accompanied by withering or chlorosis in the leaves that is not ammenable to iron supplementation. In high concentrations, particularly in low pH sods, copper can be toxic to plants. 

Copper supplements can also have an anthelmintic effect. Small amounts of copper oxide wire particles (COWP) were effective against both incoming and established Haemonchus contortus worms (Bang et al., 1990) and a mineral supplement containing elemental copper reduced faecal egg counts in lambs (Lindqvist et al., 2001). Also, Burke et al. (2004) showed a great reduction of faecal egg counts and adult worm burden of H. contortus in COWP-treated lambs. However, Dimander et al. (2003) could not show an effect against GIN in grazing cattle. 

Karring, M., R. Pohjanvirta, T. Rahko, and H. Korpela. 1981. The influence of dietary molybdenum and copper supplementation on the contents of serum uric acid and some trace elements in cocks. Acta Vet. Scand. 22 289-295. 

Ward, G.M. and J.G. Nagy. 1976. Molybdenum and copper in Colorado forages, molybdenum toxicity in deer, and copper supplementation in cattle. Pages 97-113 in W.R. Chappell and K.K. Peterson (eds.). Molybdenum in the Environment. Vol. 1. The Biology of Molybdenum. Marcel Dekker, New York. 

Tetrahymena mutants lacking functional phagocytosis require high levels of iron and copper supplements [81]. 

Two genetic disorders of copper metabolism, Wilson s disease (see Section 62.2.3.3) and Menkes disease, are known. The latter involves impaired intestinal absorption of copper56,57 as well as probably subcellular metabolic defects which result in copper deficiency with respect to metal-loenzyme activity. The characteristic steely hair in Menkes disease results from free SH bonds in hair protein because of failure of lysyl oxidase to produce the disulfide links. Depigmentation of hair and skin, hypothermia, cerebral degeneration, central nervous system retardation, skeletal demineralization and arterial degeneration are all seen. Copper supplements may benefit hypothermia and increase pigmentation but the disease is not generally cured. 

At the moment only Menkes disease, a condition which arises from an impairment of copper transport across the gut wall27, is in this category. Again, it is possible that other diseases of this nature will be identified. Suitable copper supplementation will suppress development of the disease in the foetus. The disease is characterized by progressive degeneration of the brain and the spinal cord of infants. 

Treatment As this condition is usually diagnosed in infancy, some merit can be gained from early treatment with injections (subcutaneous or intravenous) of copper supplements (acetate salts). As the condition develops additional forms of treatment may help directly address other symptoms, however, as noted earlier these merely support the individual during their reduced lifespan. 

The best known of these is the interference of copper absorption caused by zinc due to the induction of intestinal metallothionem this binds to copper and prevents its entry into the bloodstream. The intestinal cells eventually slough, carrying the copper with them. The prolonged intake of zinc necessitates copper supplements except in patients with Wilson s disease. 

ANTACIDS COPPER 4- plasma concentration of copper Most antacids will i absorption of copper If antacids are used in the long term, consider copper supplements of 1-2mg/day... 

Because copper is excreted primarily in the bile, some experts advocate reducing or curtailing copper supplementation in patients with chronic hyperbUrrubinemia. The earliest signs of copper deficiency are peripheral blood cytopenias (typically anemia and neutropenia) and occasionally thrombocytopenia, caused by reduced bone marrow production. The authors recommended that serum copper should be monitored quarterly and that copper should be included in the parenteral nutrition mixture three times a week, adjusting the frequency in response to serum copper concentrations. 

Three adult cases in which copper deficiency developed during long-term parenteral nutrition without copper supplementation have been described. All three patients were suffering from malabsorption when therapy was instituted, and overt symptoms of copper deficiency developed an average of 5.8 months after the start of parenteral nutrition. Leukopenia with neutropenia and low plasma concentrations of copper and ceruloplasmin were seen in all cases (58). 

In patients with Wilson s disease, penicillamine is rapidly attached to copper and, although higher doses are used, taste disturbances develop in a lower frequency, about 4% (SED-8, 536). It has been suggested that dysgeusia is related to deficiency of copper or zinc, but a strong connection between taste impairment and urinary copper excretion has not been demonstrated (118). Serum copper concentrations remained within normal limits and copper supplements were not effective in prevention (119). 

A 17-year-old man with anaemia, leukopenia, and neutropenia had been self-medicating with over-the-counter zinc formulations for acne for almost 2 years at doses of up to 300 mg/day (10). Serum copper and serum ceruloplasmin concentrations were less than 100 (reference range 70-155) ng/ml and 20 (23-49) pg/ml respectively. His serum zinc concentration was 2 (0.6-1.3) pg/ml. Within 1 month of withdrawal, and without copper supplementation, the ceruloplasmin concentration had risen to 90 pg/ml. By 2 months his complete blood count was normal. 

The genetic syndrome referred to as Menkes kinky hair has been studied by Williams et al. (73). No changes were observed following oral copper supplementation in plasma copper concentration or ceruloplasmin concentration in these patients. However, when copper was given intravenously, a rise in ceruloplasmin was seen. The results indicate that in Menkes syndrome, there is a defect in copper-binding protein which leads to excessive losses of copper from the gastrointestinal tract. 

Studies in these deficiency states have shed some light on the role of copper in erythropoiesis and its relationship to iron in the synthetic process. They seem to indicate that copper-containing ferroxidase is required for iron absorption and mobilization in the ferrous-to-ferric cycle oxidation. Response to copper supplementation seems to depend a great deal on whether copper deficiency is coexistent with iron deficiency or whether the deficiency has developed after iron deficiency, as evidenced by lack of erythropoietic maturation. Favorable response usually occurs in the former but not in the latter (9). 

Florida). Treatment of this condition involves copper supplementation in the feed. 

Dietary. Cp deficiency is due to nutritional copper deficiency, with secondarily low levels of Cp, and is associated with neutropenia, thrombocytopenia, low serum iron, and hypochromic, normocytic, or macrocytic anemia unresponsive to iron therapy. The deficiency may be due to inadequate dietary intake, long-term parenteral nutrition without copper supplementation, malabsorption of any cause, penicillamine therapy, or combinations of these. Therapy includes dietary change or copper supplementation, plus treatment of the primary cause of malabsorption if present. 

Nutritional Support. Adults and children fed intravenously without addition of sufficient copper to the nutrient regimen develop symptomatic copper deficiency. The hematological changes of hypochromic anemia and neutropenia are reversed by copper supplementation. Similar effects have been reported during prolonged enteral feeding via jejunostomy. Children may also develop the typical bone changes mentioned above. 

A symptom of copper deficiency in man and animals is seizures, which subside with copper supplementation [135, 305-310]. Seizures following treatment with tremor-inducing drugs are accompanied by a concomitant reduction in brain copper levels [311-314]. Also, brain norepinephrine and epinephrine concentrations are reduced in association with seizures [1, 311, 315-320]. This latter observation is particularly relevant, since two copper-dependent enzymes are required for the synthesis of norepinephrine and epinephrine. 

The observation that copper supplementation modulates the formation of arachidonic acid by regulating A -desaturase activity, which converts diho-mo-y-linolenic acid to arachidonic acid, has led to the suggestion that combinations of linoleic, y-linolenic or dibromo-y-linolenic acid with assimilable copper complexes might be useful in the treatment of inflammatory disorders, cardiovascular and thrombotic disorders, menstrual cycle disorders, diabetes, endometriosis, nutritional deficiencies and malignancies [255]. Modulation of stearoyl CoA A -desaturase activity by Cu(II)(tyrosinate)2, Cu(II)(lysinate)2, and Cu(II)(histidinate)2 [599] may also have a bearing on these uses of copper complexes. 

Green platelets. Sol in water, giving a dark -green soln. A 10% aq soln is almost neutral and can be sterilized by autoclaving. LDW i.m. in rats 126 mg/fcg (Kuzell). therap CAT Anti rheumatic. tHeRap cat (vet) Copper supplement. 

Other trace elements, particularly with zinc, were also observed indeed, high doses of zinc (40- 50 mg per day) were used successfully to treat Wilson s disease (Brewer etal. 1983). Copper supplementation protects against lead intoxication, provided that the protein status is normal (Scheinberg 1991). This finding only strengthens the notion that adequate nutrition acts as a prevention of the copper toxic-ity. 

Ruminants are quite susceptible to copper toxicity. These are the only animals in which significant, and even lethal, copper toxicity can occur without an inherited abnormality or the addition of dietary copper supplements. Copper toxicity may develop in sheep taking forage with a normal copper content of 8-10 mg kg and this is even more likely to occur if the molybdenum concentration in the diet is below 0.5 mg kg k The principal effects are on the liver and blood, with fatal hepatitis or hemolytic anemia occurring (Howell 1991a). In these respects, cattle are much like sheep (Howell 1991b). 

Ward GM and Nagy JG (1976) Molybdenum and copper in Colorado Forages. Molybdenum Toxicity in Deer and Copper Supplementation in Cattle. In ... 

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