Gestational PCB 126 exposure disrupts fetoplacental unit

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These data evidently appear that endocrine disruption by maternal PCB 126 causes several histopathological changes to the placental tissues. These alterations, in conjunction with the maternofetal body weight alterations, indicate the potential for a maternofetal hypothyroid effect with PCB 126. Additionally, the maternal PCB 126 appears to play a negative role for the fetal pituitary-thyroid axis, GH/ IGF-I axis, and cytokines levels at ED 20. Thus, maternal PCB 126 may act as a fetal thyroid-cytokines disruptor. This disturbance could decline the normal biological functions (fat metabolism) and the general health level of fetal rats. However, the toxicity of PCB 126 during the pregnancy is reliant on its concentration, duration of exposure, storage in the maternofetal biological tissues, developmental stage and the species involved. Additional studies should include the molecular, behavioral and ultrastructural analyses to explore the underlying mechanisms.

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