Copper - Nutrition

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What is Copper?

Copper belongs to the group of nutrients called the trace elements. These are essential minerals but are designated this particular description as they are required in much smaller amounts than major minerals such as calcium and phosphorus. Copper can occur in very small amounts in the free state but most copper exists as cuprous or cupric salts, with oxidation states of Cu1+ and Cu2+ respectively.

Why is it Important?

Copper has many physiological functions. It is an essential component of a number of enzymes that catalyse oxidation reactions. It is also involved in iron metabolism, energy metabolism and the formation of normal hair colour.

Roles in the Body

Each of the enzymes that requires copper can be linked to a key metabolic process and this in turn defines the essentiality of copper as a nutrient. For example, lysyl oxidase is involved in connective tissue formation while ferroxidase enzymes are involved in iron metabolism and the formation and development of red blood cells. Copper is a component of the enzyme superoxide dismutase, which is involved in protecting the body against oxidative damage. As a component of tyrosinase it is essential for the formation of the pigment melanin and therefore for normal hair colour. Copper is absorbed primarily from the small intestine; absorption is influenced by the dietary copper content, being increased when the copper intake is low. In the liver copper is bound to ceruloplasmin, which becomes the principal form of copper transported in the plasma. Iron and zinc decrease the availability of copper; zinc is a particularly potent inhibitor of copper absorption. This occurs by zinc stimulating the formation of metallothionein, a protein that has a high affinity for binding copper. Copper balance occurs mainly via biliary excretion.

Consequences of Copper Deficiency


There are few published studies on copper deficiency in dogs but signs of deficiency can be linked to the metabolic roles of copper.

Recognised Syndromes Related to Copper Deficiency

  1. Loss of hair colour and skeletal abnormalities: Zentek & Meyer fed a low dietary level of copper (1.2 mg/kg on dry matter - DM) to beagle puppies from one to six months of age. They observed a loss of hair pigmentation on the face and head after 3 months of depletion. Plasma copper concentrations began to fall after 4 weeks on the diet. After 4 months depletion hyperextension of the distal phalanges occurred[1].
  2. Reduced serum copper: Diets containing copper levels of around 4 and 8 mg/kg DM (as cupric sulphate) resulted in reduced serum copper concentrations when fed to puppies[2].


Studies of copper deficiency in cats showed different clinical signs from those observed in the dog.

Recognised Syndromes Related to Copper Deficiency

  1. Decreased weight gain and low liver concentration: Doong et al. found that kittens fed less than 4 mg/kg DM dietary copper showed signs of copper deficiency that included decreased growth rate and reduced concentrations of copper in the liver but no other consistent clinical signs[3].
  2. Effects on reproduction: In adult female cats fed low dietary copper levels (3 or 6 mg/kg DM as cupric sulphate) had an effect on reproductive efficiency, increasing the time for successful conception compared with control cats fed copper at 10 mg/kg diet. However pregnancy rates were unaffected[4][5]. This study also reported that, plasma copper levels, unlike liver copper content, did not reflect dietary copper intake.



There is a considerable amount of information on the susceptibility of certain breeds to copper hepatopathy. The disease is predominantly associated with Bedlington terriers but breeds such as the Labrador retriever, West Highland white terrier, Skye terrier and Dobermann pinscher have also been reported to be prone to this condition, which is caused by an inherited defect that results in toxic excesses of copper in the liver, causing hepatitis and cirrhosis. Affected dogs can have liver copper concentrations ten times normal values. The condition is due to a defect in the biliary excretion of copper, which is the main control of copper balance[6]. Treatment is via zinc supplementation, which reduces copper absorption, or chelating agents that increase copper excretion[7].


Unlike the dog, there appears to be little or no information on the toxic effects of copper in cats.

Dietary Sources

Copper is found in reasonable amounts in some cereal sources such as soya flour and wheat germ meal. The best animal source is liver, especially beef or lambs’ liver. There are moderate amounts in some meat meals. However, to ensure adequate dietary contents, manufactured dog and cat foods are usually supplemented with inorganic copper salts such as cupric sulphate, cupric carbonate and cupric chloride. Copper chelates of amino acids such as lysine are also good sources of bioavailable copper. However, cupric oxide is not suitable as a source of dietary copper for dogs and cats. In one study where adult cats were fed a diet containing cupric oxide as the supplement they showed clear signs of copper inadequacy, even though the dietary copper content was identical to an adequate diet where the copper was supplied by cupric sulphate[4].


  1. Zentek, J, Meyer, H (1991). “Investigations on copper deficiency in growing dogs”. J. Nutr. 121:S83-S84.
  2. Czarnecki-Maulden, G, Rudnick, R, Chausow, D (1993). “Copper bioavailability and requirement in the dog: Comparison of copper oxide and copper sulphate”. FASEB J. 7:A305.
  3. Doong, G, Keen, C, Rogers, QR, Morris, JG, Rucker, R (1983). “Selected features of copper metabolism in the cat”. J. Nutr. 113:1963-1971.
  4. 4.0 4.1 Fascetti, AJ, Morris, JG, Rogers, QR (1998). “Dietary copper influences reproductive efficiency of queens”. J Nutr. 128:2590S-2592S.
  5. Fascetti, AJ, Rogers, QR, Morris, JG (2000). “Dietary copper influences reproduction in cats”. J Nutr. 130:1287-1290.
  6. Brewer, G (1998). “Wilson’s disease and canine copper toxicosis”. Am. J. Clin. Nutr. 67(suppl.):1087S-1090S.
  7. Hyun, C, Filippich, LJ (2004). “Inherited copper toxicosis with emphasis on toxicosis in Bedlington terriers”. J. Exp. Anim. Sci. 43:39-64.

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