Fetal copper uptake and a homolog (Atp7b) of the Wilson's disease gene in rats

LEC rats are defective at the p-type copper transport ATPase gene (Atp7b) a nd exhibit excessive hepatic copper accumulation. However, copper concentra tion in fetal liver of LEC rats is lower than that of F344 normal rats. In this study, we made fetal backcrosses between LEC and F344 normal rats. At 19 days of gestation, hepatic copper concentrations of (LECXF344)F1XLEC and LECX(LECXF344)F-1 fetuses were equivalent to those of F344 and LEC fetuses , respectively, irrespective of their Atp7b genotype. Furthermore, Atp7b ex pression was identified in the uterus and the maternal portion of placenta, but not in the fetal portion of placenta, in pregnant F344 rats. From thes e results, we speculate that the Atp7b product might contribute to a copper transport system from mother to fetus in the maternal portion, but not in the fetal portion of placenta.