Copper deficiency symptoms

About 50% of copper in food is absorbed, usually under equitibrium conditions, and stored in the tiver and muscles. Excretion is mainly via the bile, and only a few percent of the absorbed amount is found in urine. The excretion of copper from the human body is influenced by molybdenum. A low molybdenum concentration in the diet causes a low excretion of copper, and a high intake results in a considerable increase in copper excretion (68). This copper—molybdenum relationship appears to correlate with copper deficiency symptoms in cattle. It has been suggested that, at the pH of the intestine, copper and molybdate ions react to form biologically unavailable copper molybdate (69). 

The extent of the adverse effect of high sulfur intake in the diet of animals depends on species, the source of sulfur, and the concentration in feedstuffs. After depletion of the copper storages of the body, a sulfur exposure causes a secondary copper deficiency, especially in ruminants. In practice, it is difficult to distinguish between direct sulfur-induced toxic effects and secondary copper deficiency symptoms. 

Absorption, Metabolism, Excretion Functions of Copper Deficiency Symptoms Interrelationships... 

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. 

Two inherited human diseases that represent abnormal copper metabolism are Menkes syndrome and Wilson s disease. Menkes syndrome, with symptoms similar to those of copper deficiency, is characterized by a progressive brain disease, abnormally low copper concentrations in liver and other tissues, and diminished ability to transfer copper across the absorptive cells of the intestinal mucosa (USEPA 1980 Aaseth and Norseth 1986). Wilson s disease (hepatolenticular degeneration) is the only significant example of copper toxicity in humans. Wilson s disease is an autosomal recessive disorder that affects normal copper homeostasis and is characterized by excessive... 

Large amounts of copper are found in the liver, larger amounts in young individuals than in old. In cases of copper deficiency, anemia, hair discoloration, and other pathological symptoms have been observed. Increased levels of copper, which result from defense mechanism actions of the immune system, have been reported in infectious and cancer diseases (Sarkar, 1995). 

Ruminants are sensitive to copper deficiency. The symptoms ol copper deficiency in animals vary with ihe species and age. but often the fading... 

A second example of cluster formation involves the antagonism between molybdenum and copper. The presence of high concentrations of molybdenum in pasture soils is known to lead to symptoms of copper deficiency in animals. This has been attributed to the formation of thiomolyb-dates in the rumen of grazing animals, which then interfere with the metabolism of copper through the formation of cluster compounds of molybdenum and copper. It has been shown that thiomolyb-date, MoS42, readily forms such clusters on reaction with phosphines and copper(II) salts under appropriate conditions. Structures are shown in Figure 38.992,993 Reaction between thiomolybdate and copper compounds in aqueous solution have also been reported.994... 

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... 

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). 

Various nutrient deficiencies can affect lettuce. Boron or phosphorus deficiency causes malformed plants. Calcium deficiency causes browning of young leaves. Poor heart formation is a symptom of molybdenum deficiency. Copper deficiency prevents heads from forming. Spray seedlings with seaweed extract to help prevent nutrient deficiencies. Continue to spray plants with seaweed extract or compost tea every 2 weeks to boost plant health. Do a soil test to confirm the deficiency, and amend soil accordingly. 

Table IV. Effects of Ascorbic Acid on Symptoms of Copper Deficiency in Dutch Rabbits Fed Low-Copper Diets...

Since the zinc-copper ratio is important, intake of too much zinc can lead to symptoms of copper deficiency. However, patients have taken 10 times the recommended daily allowance for zinc with no adverse reaction. 

Copper is a cofactor in several enzymes, including lysyl oxidase and superoxide dismutase. Ceruloplasmin, a deep-blue glycoprotein, is the principal copper-containing protein in blood. It is used to transport Cu2+ and maintain appropriate levels of Cu2+ in the body s tissues. Ceruloplasmin also catalyzes the oxidation of Fe2+ to Fe3+, an important reaction in iron metabolism. Because the metal is widely found in foods, copper deficiency is rare in humans. Deficiency symptoms include anemia, leukopenia (reduction in blood levels of white blood cells), bone defects, and weakened arterial walls. The body is partially protected from exposure to excessive copper (and several other metals) by metal-lothionein, a small, metal-binding protein that possesses a large proportion of cysteine residues. Certain metals (most notably zinc and cadmium) induce the synthesis of metallothionein in the intestine and liver. 

Individuals who are at risk for copper deficiency include people who are recovering from abdominal surgery, which causes decreased absorption of copper from the intestine. Others at risk are premature babies and people who are sustained solely by intravenous feedings that are deficient in copper. In addition, people who ingest high doses of antacids or take excessive supplements of zinc, iron, or vitamin C can develop copper deficiency because of reduced copper absorption. Because copper is involved in so many processes in the body, it is not surprising that the symptoms of copper deficiency are many and diverse. They include anemia decreased red and white blood cell coimts heart disease increased levels of serum cholesterol loss of bone defects in the nervous system, im-mime system, and connective tissue and abnormal hair. 

Both children and adults can develop symptomatic copper deficiency. Premature infants are the most susceptible since copper stores in the liver are laid down in the third trimester of pregnancy. In adults, deficiency is usually found following inicsiinul bypass surgery or in patients on parenteral nutrition. Symptoms range from bone disease to an iron-resistant microcytic hypochromic anaemia. 

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. 

Chronic leukaemia is associated with a near-normal plasma copper concentration and a markedly decreased hematocrit, which may be symptoms of copper deficiency. Since remissions do not occur in cases of chronic lymphocytic and myeloid leukaemias as well as myelomas, serum copper levels do not return to normal [332]. 

Anke M, MasaokaT, Schmidt A and Arnhold W (1988) Antagonistic effects of a hi sulphur, molybdenum and cadmium content of diets on copper metabolism and deficiency symptoms in cattle andpi. In Hurley LS, et al., eds. Trace Element in Man and Animals - 6, pp. 317-318. 

In contrast to its essentiality, every element of the periodic system may be toxic it is only a question of the intake quantities and the element specification. An intoxication can induce interactions with essential elements and induce deficiency symptoms well-known examples are the interactions of nickel with zinc, magnesium, and manganese (Anke etal. 19971), or cadmium with copper, zinc, and iron (Anke et al 1970). 

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