Modifier of Copper Toxicosis

Body function:

Hormonal & Endocrine

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Copper toxicosis related to the ATP7A gene is a genetic trait that influences how copper is processed in dogs, specifically Labrador Retrievers. Copper toxicosis is a condition where copper accumulates in the liver, potentially causing damage and cirrhosis over time. This condition is primarily linked to mutations in the ATP7B gene, but other genes, including ATP7A, can also modify how copper is metabolized. The ATP7A gene mutation can decrease copper accumulation, acting as a protective factor for dogs that are also carriers of the ATP7B mutation. Male dogs who inherit only one copy of the APT7A gene tend to show more noticeable copper level reductions, while females need two copies for the same effect.

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List of affected breeds:

Genetic research has linked this gene and condition in the following breeds:

Labrador Retriever

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What does this mean for a dog with this trait?

Managing copper toxicosis involves combining dietary management and regular vet care to reduce copper accumulation in the liver. ATP7A mutations can have a protective effect on copper levels, which are beneficial for the dog. However, testing for all relevant gene mutations (ATP7A, ATP7B, and RETN) is essential to tailor an effective treatment strategy.

Symptoms

Dogs with copper toxicosis often begin to show symptoms around middle age. Initial signs may include weight loss, weakness, lethargy, vomiting, diarrhea, and abdominal pain, but symptoms are likely to become more severe as the disease progresses. However, the presence of ATP7A mutations may lead to a milder form of the disease or delay the onset of symptoms in dogs carrying the ATP7B mutation.

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