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首页> 外文期刊>Reproductive toxicology >Developmental dioxin exposure of either parent is associated with an increased risk of preterm birth in adult mice.
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Developmental dioxin exposure of either parent is associated with an increased risk of preterm birth in adult mice.

机译：任一亲本的发育性二恶英暴露都与成年小鼠早产风险增加有关。

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We have previously described diminished uterine progesterone response and increased uterine sensitivity to inflammation in adult female mice with a history of developmental exposure to TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin). Since parturition in mammals is an inflammatory process mediated in part by a decline in progesterone action, toxicant-mediated disruption of progesterone receptor (PR) expression at the maternal-fetal interface would likely impact the timing of birth. Therefore, in the current study, we examined pregnancy outcomes in adult female mice with a similar in utero exposure to TCDD. We also examined the impact of in utero TCDD exposure of male mice on pregnancy outcomes in unexposed females since the placenta, a largely paternally derived organ, plays a major role in the timing of normal parturition via inflammatory signaling. Our studies indicate that developmental exposure of either parent to TCDD is associated with preterm birth in a subsequent adult pregnancy due to altered PR expression and placental inflammation.
机译：我们先前描述了成年雌性小鼠的子宫孕酮反应减弱，子宫对炎症的敏感性增加，这些雌性小鼠有接触TCDD（2,3,7,8-四氯二苯并-p-二恶英）的发展史。由于哺乳动物的分娩是部分由黄体酮作用下降引起的炎症过程，因此在母体-胎儿界面上由毒物介导的黄体酮受体（PR）表达破坏可能会影响出生时间。因此，在本研究中，我们检查了子宫内TCDD暴露量相似的成年雌性小鼠的妊娠结局。我们还检查了雄性小鼠子宫内TCDD暴露对未暴露雌性妊娠结局的影响，因为胎盘是一种主要由父系衍生的器官，通过炎症信号在正常分娩的时间中起着重要作用。我们的研究表明，由于PR表达和胎盘炎症的改变，任何一位父母的TCDD发育暴露与​​随后的成年妊娠中的早产有关。

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