Developmental dioxin exposure of either parent is associated with an increased risk of preterm birth in adult mice.

Ding T, McConaha M, Boyd KL, Osteen KG, Bruner-Tran KL
Reprod Toxicol. 2011 31 (3): 351-8

PMID: 21093581 · PMCID: PMC3075349 · DOI:10.1016/j.reprotox.2010.11.003

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.

Copyright © 2010 Elsevier Inc. All rights reserved.

MeSH Terms (18)

Animals Epigenesis, Genetic Female Gene Expression Male Maternal Exposure Mice Mice, Inbred C57BL Paternal Exposure Placenta Placenta Diseases Polychlorinated Dibenzodioxins Pregnancy Premature Birth Prenatal Exposure Delayed Effects Receptors, Progesterone RNA, Messenger Teratogens

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