Exposure to 2,2′,4,4′-tetrabromodiphenyl ether at late gestation modulates placental signaling molecules in the mouse model

- Exposure to 2,2′,4,4′-Tetrabromodiphenyl ether increased incidence of low birth weight and stillbirth in mice.
- Mitogen-activated protein kinases were induced by the pollutant administration.
- Placental growth hormone and some steroid hormones in maternal plasma were reduced.

Polybrominated diphenyl ethers (PBDEs) are flame retardants generally employed in manufacturing household items. Surface water may remove and carry these chemicals to the drainage upon disposal of the items, and ultimately the chemicals enter our food chain. 2,2′,4,4′-Tetrabromodiphenyl ether (BDE-47) is a PBDE congener commonly found in contaminated seafood. The placenta is the site of nutrient exchange and is responsible for reproductive hormone secretion during pregnancy. In the present study, pregnant ICR mice were given p.o. daily doses of BDE-47 at 0, 0.36, 3.6, 36 mg/kg for 4 days (from E13.5 to E16.5). Compared to the control group, increased rates of stillborn and low birth weight were observed in mice treated with 36 mg BDE-47/kg. Plasma testosterone and progesterone levels were reduced in mice treated with 36 mg BDE-47/kg. In addition, the group treated with 3.6 mg/kg of BDE-47 displayed decreased growth hormone (Gh) peptide expression in the placental tissue extracted at E17.5. As this peptide stimulates growth, the expression pattern might suggest compromised fetal development. Further analysis indicated that mitogen-activated protein kinases (MAPK) were activated in the placental tissue of the BDE-47-treatment groups. The activation of these signaling molecules might affect the hormonal and other physiological functions in the tissue.