A disorder of copper metabolism, due to a deficiency of ceruloplasmin, which forms a complex with copper. The excess copper is deposited in the brain (causing mental retardation) or the liver (causing jaundice and cirrhosis). The primary cause of copper toxicosis in Labrador Retrievers is a mutant form of ATP7B. Dogs that inherit two normal versions of the gene (one from each parent) will have normal levels of copper in their livers. Dogs that inherit one normal copy and one mutant copy will have somewhat elevated levels of copper in their liver, while those that inherit two mutant copies will have the highest levels. A second gene involved in the Labrador disease is a mutated form of ATP7A. This mutation helps minimize the accumulation of copper in the liver, and is X-linked Recessive. Males only need to inherit one copy of the mutant gene to help with their copper levels, while females need to inherit two. See also: Menkes Disease.