Gestational exposure to PCB-118 impairs placental angiogenesis and fetal growth

Maternal exposure to polychlorinated biphenyls (PCBs) results in adverse effects on fetal development. However, the underlying mechanism has not been sufficiently explored in respect to particular PCBs. Placental angiogenesis plays a crucial role in feto-maternal substances transportation and fetal development. The present study was conducted to investigate the effects of prenatal PCB118 exposure on placental angiogenesis and fetal growth. The pregnant dam received PCB118 at environmentally relevant doses (0, 20, or 100 mu g/kg/day) intragastrically from gestational day (GD) 7.5-18.5 to establish an in vivo model. Compared with the control group, the fetal body and placental weights of the PCB118 (100 mu g/kg/day) group were significantly decreased and the intrauterine growth retardation (IUGR) rates were increased both in the female and male fetus. Furthermore, we found that placental histology was significantly impaired and the number of blood vessels was decreased in the PCB118 group. Additionally, gestational exposure to PCB118 caused anomalous mRNA expression of the genes in the placenta regarding angiogenesis. These findings indicate that PCB118 may contribute to the occurrence of IUGR by provoking placental angiogenesis dysfunction. This study clarified the adverse effects and potential mechanism of prenatal PCBs exposure on fetal growth, providing a new theoretical and experimental basis for future treatment and prevention.

Automated summary

Maternal exposure to PCB118 was found to have adverse effects on placental angiogenesis and fetal growth. PCB118 exposure caused decreased fetal body and placental weights, increased rates of intrauterine growth retardation (IUGR), impaired placental histology, decreased number of blood vessels, and anomalous mRNA expression of genes related to angiogenesis in the placenta.