Copper [Cu, 29]
105
Cu enzymes, ceruloplasmin (feroxidase I and feroxidase II) has the ability to oxidize
Fe 2+ to Fe 3+ , which are connected to the protein transferring, for the transportation to
red blood cells, and blood formation (Angelova et al. 2011).
A number of reactions essential to normal function of the brain and nervous system are catalyzed by Cu enzymes. The Cu enzyme, tyrosinase, is required for the
formation of the pigment melanin. Melanin is formed in cells called melanocytes
and plays a role in the pigmentation of the hair, skin, and eyes.
Deficiency or excess of Cu in the organism is observed in metabolic disturbances
and in various diseases and conditions. Diseases with too low concentrations of Cu
are Menkes syndrome, Parkinson’s disease, protein loss, nephrosis, exudative enteropathy, and others.
There are two well-known genetic diseases affecting Cu metabolism, Menkes
and Wilson diseases. Menkes kinky-hair disease is a problem with Cu transport or
absorption. Wilson’s disease is characterized by increased liver Cu content, leading to severe hepatic damage, followed by increased brain Cu levels and neurological problems. Menkes disease results in pathology resembling Cu deficiency, as
opposed to the pathology of Wilson’s disease, which resembles Cu toxicity (Stern
et al. 2007).
Dietary interactions of Cu with sucrose or fructose, animal proteins, S-amino
acids, histidine, and ferrous iron may inhibit Cu absorption to varying degrees, in
animal models. Ascorbic acid supplements, Mo and other dietary factors, specifically high intakes of Ca and/or P and Cd, may also inhibit Cu absorption in diets
containing high amounts of compounds. The interaction between Zn and Cu is well
documented in humans. High levels of dietary Zn adversely influence the Cu absorption and bioavailability (SCF 2003).
Provisional maximum tolerable daily intake established for Cu is 0.05–0.5 mg/kg bw
(WHO 1982a), and estimated safe and adequate daily dietary intakes is 1.5 ± 3.0 mg
(WHO 2004). In the EU countries, it has been recommended that adult males and females
should consume a dietary intake of 0.9 mg Cu/day (SCF 2003). The main sources of Cu
in diets are cereals and cereal products, vegetables, and potatoes (Table 14.3).
Mean dietary Cu intakes from food of adults in various EU countries have been
estimated within the range of 1.0–2.3  mg/day for males, and 0.9–1.8  mg/day for
females. Vegetarian diets provided greater dietary intakes of Cu, approximately
2.1–3.9 mg/day (SCF 2003).
14.7 ANIMALS
The livestock, cattle and sheep, commonly show indications when they are Cu deficient. Swayback, a sheep disease associated with Cu deficiency, imposes enormous
costs on farmers worldwide, particularly in the Europe, the United States, and many
tropical countries.
Copper is responsible for many functions in the animals, of which one is hemoglobin formation. Copper also plays a role in bone cell function, pigment production,
hair, hoof and horn formation, and animal growth.
Signs and symptoms of Cu deficiency include change in hair coat color, diarrhea,
decreased weight gain, unthrifty appearance, anemia, fractures, lameness, decreased