Was ist Kupferspeicherkrankheit beim Hund?

Kupferspeicherkrankheit ist die Akkumulation von Kupfer in der Leber mit folgendem chronischen Leberschaden. Beim Bedlington Terrier durch COMMD1-Genmutation. Auch Dobermann, Labrador und Dalmatiner betroffen.

Wie behandelt man Kupferspeicherkrankheit beim Hund?

Kupferchelatoren (D-Penicillamin, Trientine) fördern die Ausscheidung. Zinksupplementation verhindert neue Resorption. Kupferarme Diät als Dauermaßnahme — kein Leber täglich, keine Meeresfrüchte regelmäßig.

Wie viel Kupfer braucht ein Hund täglich?

AAFCO-Minimum: 7,3 mg/kg Trockenmasse. Kommerzielles Fertigfutter deckt den Bedarf sicher. Bei BARF mit viel Leber oder kupferreichen Zutaten kann der sichere Bereich überschritten werden.

Nutrition & Nutrients

Copper in Dogs: Function, Requirements, and Copper Storage Disease

Copper (Cu) is an essential trace element that dogs must obtain through their diet. As a cofactor for numerous enzymes, copper is involved in energy production (cytochrome c oxidase), collagen synthesis (lysyl oxidase), antioxidant protection (superoxide dismutase), pigmentation (melanin synthesis), and iron utilization (ceruloplasmin).

Auf einen Blick

Copper (Cu) is an essential trace element that dogs must obtain through their diet. As a cofactor for numerous enzymes, copper is involved in energy production (cytochrome c oxidase), collagen synthesis (lysyl oxidase), antioxidant protection (superoxide dismutase), pigmentation (melanin synthesis), and iron utilization (ceruloplasmin).
Risiko-Hinweis: low-medium: Consider context and individual differences
Wissenschaftliche Einordnung: NRC (2006, Nutrient Requirements of Dogs and Cats) defines copper requirements and safety limits: AAFCO minimum for adult dogs: 7.3 mg/kg dry matter. NRC upper limit (maximum tolerable intake): 250 mg/kg DM. Copper is primarily excreted via the liver and bile—in cases of genetically impaired biliary excretion, copper accumulates in hepatocytes, causing oxidative cell damage. Zinc competes with copper for intestinal absorption (metallothionein)—high zinc intake reduces copper absorption.Fascetti and Delaney (2012, Applied Veterinary Clinical Nutrition) describe nutritional therapeutic approaches for copper storage disease: A low-copper diet (avoidance of copper-rich foods such as liver, shellfish, crustaceans, nuts, legumes) slows copper accumulation. Zinc supplementation (zinc acetate or zinc sulfate) inhibits intestinal copper absorption by inducing metallothionein in enterocytes. D-penicillamine or trientine (copper chelators) mobilize hepatic copper and promote renal excretion—standard medicinal therapy.van De Sluis et al. (2002, Human Molecular Genetics, https://pubmed.ncbi.nlm.nih.gov/11809726/) identified the MURR1 gene (later COMMD1) through positional cloning in Bedlington Terriers as a novel copper metabolism gene: The genetic defect in the COMMD1 gene (autosomal recessive) leads to defective biliary copper excretion in Bedlington Terriers. The COMMD1 protein is a negative regulator of the copper transporter ATP7B—in COMMD1 deficiency, copper progressively accumulates in hepatocytes. A DNA test for the COMMD1 mutation is available for Bedlington Terriers and is a standard for breeding health.

Copper in Dogs: Function, Requirements, and Copper Storage Disease

What is copper poisoning in dogs?

Copper (Cu) is an essential trace element that dogs must obtain from their diet. As a cofactor for numerous enzymes, copper plays a role in energy production (cytochrome c oxidase), collagen synthesis (lysyl oxidase), antioxidant protection (superoxide dismutase), pigmentation (melanin synthesis), and iron utilization (ceruloplasmin).

Copper is the only trace element in dogs that can be stored in clinically significant amounts—primarily in the liver. In certain breeds, this process is genetically dysregulated, leading to life-threatening copper storage disease.

Background + Scientific Context

The NRC (2006, *Nutrient Requirements of Dogs and Cats*) defines copper requirements and safety limits: AAFCO minimum for adult dogs: 7.3 mg/kg dry matter. NRC upper limit (maximum tolerable intake): 250 mg/kg DM. Copper is primarily excreted via the liver and bile—in cases of genetically impaired biliary excretion, copper accumulates in hepatocytes and causes oxidative cell damage. Zinc competes with copper for intestinal absorption (metallothionein)—high zinc intake reduces copper absorption.

Fascetti and Delaney (2012, *Applied Veterinary Clinical Nutrition*) describe nutritional therapeutic approaches for copper storage disease: A low-copper diet (avoiding copper-rich foods such as liver, shellfish, nuts, and legumes) slows down copper accumulation. Zinc supplementation (zinc acetate or zinc sulfate) inhibits intestinal copper absorption by inducing metallothionein in enterocytes. D-penicillamine or trientine (copper chelators) mobilize hepatic copper and promote renal excretion—standard drug therapy.

van De Sluis et al. (2002, Human Molecular Genetics, https://pubmed.ncbi.nlm.nih.gov/11809726/) identified the MURR1 gene (later COMMD1) through positional cloning in Bedlington Terriers as a new copper metabolism gene: The genetic defect in the COMMD1 gene (autosomal recessive) leads to defective biliary copper excretion in Bedlington Terriers. The COMMD1 protein is a negative regulator of the copper transporter ATP7B—in the presence of a COMMD1 deficiency, copper progressively accumulates in hepatocytes. DNA testing for the COMMD1 mutation is available for Bedlington Terriers and is standard practice in breeding programs.

Vitomalia-Position

Copper in regular Dog Food is not a problem—on the contrary, deficiency is extremely rare in dogs fed commercial dog food. Copper becomes an issue in three scenarios: breeds with genetic copper storage disorders, extreme supplementation or a diet high in copper, and BARF diets with a very high proportion of liver. Copper storage disorders require lifelong dietary and medical treatment.

When does copper become relevant?

Breeds prone to the condition (Bedlington Terrier, Doberman, Labrador Retriever, Dalmatian)
Elevated liver enzymes with no other identifiable cause → Check copper metabolism
BARF diets with a high proportion of liver (liver = the food richest in copper)
Zinc deficiency can contribute to a secondary copper excess
DNA Testing for Bedlington Terriers Before Breeding

Practical application

Copper content of selected foods:

Food	copper content	Rating
Beef liver	14 mg/100 g	Very high (limit!)
chicken liver	0.5 mg/100 g	Moderate
Beef (muscle)	0.1 mg/100 g	Low
Shrimp	0.3 mg/100 g	Moderate
Cashews	2.2 mg/100 g	High (not for Dog Food)
Potatoes	0.1 mg/100 g	Low

Copper storage disease — affected breeds: - Bedlington Terrier: COMMD1 mutation (well characterized, DNA test available) - Doberman Pinscher: Copper-induced hepatitis is common in dogs over 3 years of age - Labrador Retriever: growing awareness of copper-associated hepatitis - Dalmatian, WHWT, Skye Terrier: documented increased risk

Treatment options for copper storage disease: - D-penicillamine: copper chelation → renal excretion (side effects: vomiting, kidney damage) - Trientine: An alternative chelation therapy with fewer side effects - Zinc supplementation: prevents copper reabsorption (prevention/maintenance) - Low-copper diet: Avoid liver, shellfish, and nuts

Common Mistakes & Myths

"Liver is healthy for dogs—but daily consumption isn't recommended." Liver is very high in copper (and vitamin A)—daily feeding can quickly exceed safe copper levels, especially for breeds that are sensitive to copper. Occasional feeding (1–2 times a week in small amounts) is safe for healthy dogs.
“Copper storage disease is usually detected early.” The disease remains clinically silent for years. Liver enzymes may not rise until there is significant liver damage. Screening via liver biopsy or DNA testing is recommended for predisposed breeds.
“Zinc and copper are mutually exclusive.” They compete for absorption—but this can be harnessed in a controlled manner: zinc supplementation as a therapeutic approach for copper storage disorders reduces copper absorption without leading to critical deficiencies.

Current State of Research (2026)

Copper metabolism in dogs is well characterized, particularly the genetic basis of copper storage disease. DNA testing for COMMD1 mutations is established as a standard practice in Bedlington Terrier breeding. Current research is investigating copper hepatitis phenotypes in other breeds (particularly Labradors) and optimized dietary copper limits in commercial diets. Commercial low-copper diets are available for predisposed breeds.

Frequently Asked Questions

What is copper storage disease in dogs?

Copper storage disease is a condition in which copper accumulates in the liver, leading to chronic hepatitis and cirrhosis. In Bedlington Terriers, it is caused by a genetic defect (COMMD1 mutation). Other affected breeds include the Doberman, Labrador, and Dalmatian.

How is copper storage disease treated in dogs?

Copper chelators (D-penicillamine, trientine) promote copper excretion. Zinc supplementation prevents further copper absorption. A low-copper diet (no large amounts of liver, no daily seafood) as a long-term measure.

How much copper does a dog need each day?

AAFCO minimum: 7.3 mg/kg dry matter. Copper deficiency is extremely rare in dogs fed commercial dog food—their needs are easily met. With a BARF diet that includes a lot of liver or seaweed, their needs may be slightly exceeded.

Related terms

Sources & Further Reading

National Research Council (NRC). (2006). Nutrient Requirements of Dogs and Cats. National Academies Press. ISBN 9780309086288.
Fascetti, A. J., & Delaney, S. J. (Eds.) (2012). Applied Veterinary Clinical Nutrition. Wiley-Blackwell. ISBN 9780813815688.
van De Sluis, B., Rothuizen, J., Pearson, P. L., van Oost, B. A., & Wijmenga, C. (2002). Identification of a new copper metabolism gene by positional cloning in a purebred dog population. Human Molecular Genetics, 11(2), 165–173. https://pubmed.ncbi.nlm.nih.gov/11809726/

Wissenschaftliche Einordnung

NRC (2006, Nutrient Requirements of Dogs and Cats) defines copper requirements and safety limits: AAFCO minimum for adult dogs: 7.3 mg/kg dry matter. NRC upper limit (maximum tolerable intake): 250 mg/kg DM. Copper is primarily excreted via the liver and bile—in cases of genetically impaired biliary excretion, copper accumulates in hepatocytes, causing oxidative cell damage. Zinc competes with copper for intestinal absorption (metallothionein)—high zinc intake reduces copper absorption.

Fascetti and Delaney (2012, Applied Veterinary Clinical Nutrition) describe nutritional therapeutic approaches for copper storage disease: A low-copper diet (avoidance of copper-rich foods such as liver, shellfish, crustaceans, nuts, legumes) slows copper accumulation. Zinc supplementation (zinc acetate or zinc sulfate) inhibits intestinal copper absorption by inducing metallothionein in enterocytes. D-penicillamine or trientine (copper chelators) mobilize hepatic copper and promote renal excretion—standard medicinal therapy.

van De Sluis et al. (2002, Human Molecular Genetics, https://pubmed.ncbi.nlm.nih.gov/11809726/) identified the MURR1 gene (later COMMD1) through positional cloning in Bedlington Terriers as a novel copper metabolism gene: The genetic defect in the COMMD1 gene (autosomal recessive) leads to defective biliary copper excretion in Bedlington Terriers. The COMMD1 protein is a negative regulator of the copper transporter ATP7B—in COMMD1 deficiency, copper progressively accumulates in hepatocytes. A DNA test for the COMMD1 mutation is available for Bedlington Terriers and is a standard for breeding health.