Document Detail

Developmental dioxin exposure of either parent is associated with an increased risk of preterm birth in adult mice.
MedLine Citation:
PMID:  21093581     Owner:  NLM     Status:  MEDLINE    
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.
Tianbing Ding; Melinda McConaha; Kelli L Boyd; Kevin G Osteen; Kaylon L Bruner-Tran
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-11-18
Journal Detail:
Title:  Reproductive toxicology (Elmsford, N.Y.)     Volume:  31     ISSN:  1873-1708     ISO Abbreviation:  Reprod. Toxicol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-12     Completed Date:  2011-07-26     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  8803591     Medline TA:  Reprod Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  351-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Epigenesis, Genetic / drug effects*
Gene Expression / drug effects
Maternal Exposure / adverse effects*
Mice, Inbred C57BL
Paternal Exposure / adverse effects*
Placenta / drug effects,  metabolism,  pathology
Placenta Diseases / chemically induced,  metabolism,  pathology
Premature Birth / chemically induced*
Prenatal Exposure Delayed Effects / chemically induced*
RNA, Messenger / metabolism
Receptors, Progesterone / genetics,  metabolism
Teratogens / toxicity*
Tetrachlorodibenzodioxin / toxicity*
Grant Support
R01 ES014942/ES/NIEHS NIH HHS; R01 ES014942-01/ES/NIEHS NIH HHS; R01ES14942/ES/NIEHS NIH HHS; R21 AT006245/AT/NCCAM NIH HHS; R21 AT006245-01/AT/NCCAM NIH HHS; R21 AT006245-02/AT/NCCAM NIH HHS; R21AT006245-01/AT/NCCAM NIH HHS
Reg. No./Substance:
0/RNA, Messenger; 0/Receptors, Progesterone; 0/Teratogens; DO80M48B6O/Tetrachlorodibenzodioxin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Astrocytes support hippocampal-dependent memory and long-term potentiation via interleukin-1 signali...
Next Document:  Distribution of orexinergic neurons and their terminal networks in the brains of two species of Afri...