Evaluation of COMMD1 in copper toxicosis in Labrador retrievers and Dobermans

Abstract

Copper toxicosis is a major cause of hepatitis in dogs. We have shown that variants in ATP7A and ATP7B modulate hepatic copper levels in Labrador retrievers and Dobermans. However, these variants cannot fully explain the observed variation in hepatic copper levels in these dog breeds. Homozygous deletion of exon 2 of COMMD1 causes copper toxicosis in Bedlington terriers. We investigated the possible involvement of COMMD1 in the multifactorial aetiology of copper toxicosis in Labrador retrievers and Dobermans. Thirty dogs of each breed with known hepatic copper status were selected for DNA sequence analysis of the three exons and flanking intronic regions of COMMD1. The observed variants were tested for association with hepatic copper levels by linear model analysis. Several variants were observed in the DNA sequence of COMMD1 in both Labrador retrievers (nine variants) and Dobermans (11 variants) but none of these was associated with variations of hepatic copper concentrations. We conclude that COMMD1 did not play a major role in the aetiology of copper associated hepatitis in Labrador retrievers and Dobermans.