Copper deficiency during pregnancy results in embryonic and fetal abnormalities as well as persistant effects on postnatal development. The long term objective of these studies is to understand the mechanisms of copper deficiency-induced abnormalities on embryonic development. The investigators will focus on oxidative mechanisms at a morphologic and mechanistic level the abnormalities in cardiovascular integrity observed in copper deficient embryos. In vitro culture methods will be used to elucidate the mechanisms by which copper-induced alterations in extracellular matrix modulate vascular growth and differentiation during blood vessel assembly. Furthermore, the investigators will study the role of select proteins in intracellular copper transport and metabolism in embryonic development using antisense technology. This information should provide new insights into the mechanisms underlying copper deficient pathologies and may contribute to our understanding of this process during human development.