Placenta exchanges vital factors including oxygen, carbon dioxide, cation(copper, iron, calcium) and glucose that are essential to fetal growth. Copper, iron, calcium cation and glucose transfer genes are regulated by reproduction-related hormones, vitamin D and human placental lactogen. These molecules are transferred by specific receptors located on cell membrane or cytoplasm in placenta. These substances disturb action of reproduction-related hormones (ex> estrogen, progesterone) by interacting with their receptors, or affecting the expression of transporting genes for cations. To examine the effects of EDCs exposure during pregnancy, we conducted the in vivo model study using Pregnancy mouse. We used different doses of octyl-phenol (OP; 50 mg/kg/day), and bisphenol A (BPA; 50 mg/kg/day) in pregnancy mice for GD 11.5~16.5. Ethinyl estradiol (EE; 0.2 mg/kg/day), which activates estrogen receptors, was used as a positive control. ICI 182 780(70 ug/kg) were used with estrogen antagonist. Transcription of calcium transporting genes, copper transporting genes, and iron transporting genes was quantified by qRT-PCR. Treatment with EE, OP, BPA in a mouse placenta affected expression of calcium transporting genes (PMCA1, TRPV6), copper transporting genes (CTR1, ATP7A), and iron transporting genes (IREG1, HEPH). Expression of the gene was confirmed in the control group and the experimental group. In the result of real-time PCR, relative mRNA expression levels of PMCA1, TRPV6, ATP7A, CTR1, HEPH, IREG1 in some group were decreased or increase compared to the vehicle control. We concluded essential cation transporting genes in placenta are modulated by EDCs.