Overview

• Important trace mineral.
• Serves as a cofactor for enzymes involved in many biologic processes.
• In plasma, 95% bound to cerulplasmin (α2 globulin).
• Excess copper accumulates in hepatocytes.
• Hepatocellular damage, generally secondary to stress, releases hepatocellular copper stores into the bloodstream, leading to acute hemolysis.
• Death results from acute hemolytic crisis.
• Copper deficiency may occur with diets high in molybdenum. Clinical signs include decreased growth, poor coat, bone abnormalities and anemia.
• Copper deficiency and copper toxicosis are rare in clinical practice.

Sampling

Tests

Availability

• Contact commercial laboratory to confirm availability.
• Liver tissue sample generally preferred for copper analysis.

Technique (intrinsic) limitations

• Test results only significant in conjunction with other laboratory results and clinical findings.

Result Data

Further Reading

Publications

Refereed Papers

• Recent references from PubMed and VetMedResource.
• Ramirez C J, Kim D Y, Hanks B C & Evans T J (2013) Copper toxicosis in New Zealand White Rabbits (Oryctolagus cuniculus). Vet Pathol 50 (6), 1135-1138 PubMed.
• Cooper G L et al (1996) Copper poisoning in rabbits associated with acute intravascular hemolysis. J Vet Diag Invest 8 (3), 394-396 PubMed.

Other sources of information

• Meredith A (2014) Dermatoses. In: Manual of Rabbit Medicine. Eds: Meredith A & Lord B. BSAVA. pp 255-263.
• Prebble J (2014) Nutrition and Feeding. In: Manual of Rabbit Medicine. Eds: Meredith A & Lord B. BSAVA. pp 27-35.