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Evidence is accumulating that copper is a cause of liver disease in breeds of dogs other than Bedlington terriers.
Atox1 is therefore excluded as a candidate gene for canine copper toxicosis, indicating that some other unidentified gene must be responsible for this copper storage disease in dogs and also suggesting the possibility of a similar gene responsible for a copper storage disease in humans.
This study revealed an excellent treatment response of dogs with hepatic copper accumulation to feeding of a copper-restricted diet.
Our results demonstrate that copper toxicosis in Bedlington terriers is not an animal model for the non-Wilsonian hepatic copper toxicosis described in this study.

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