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HERO ID
4728734
Reference Type
Journal Article
Title
The effect of maternal exposure to di-(2-ethylhexyl)-phthalate on fetal cardiac development in mice
Author(s)
Tang, C; Deng, Y; Duan, H; Zhang, Y; Li, Y; Qiu, D; Zhou, K; Hua, Y; Wang, C
Year
2018
Is Peer Reviewed?
Yes
Journal
Journal of Applied Toxicology
ISSN:
0260-437X
EISSN:
1099-1263
Publisher
John Wiley and Sons Ltd
Volume
38
Issue
6
Page Numbers
834-842
Language
English
PMID
29377175
DOI
10.1002/jat.3591
Web of Science Id
WOS:000430177900005
URL
https://search.proquest.com/docview/2025907048?accountid=171501
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Abstract
Accumulating evidence has suggested a link between maternal di-(2-ethylhexyl)-phthalate (DEHP) exposure and various developmental abnormalities. However, the evidence regarding the effect of maternal DEHP exposure on fetal cardiac development is scarce. The present study aimed to determine the effect of maternal DEHP exposure on fetal cardiac development in mice and explore the possible involved mechanism preliminarily. The C57BL mice were randomly divided into four groups: the vehicle group (corn oil, n = 10), 250 mg kg-1 DEHP group (n = 15), 500 mg kg-1 DEHP group (n = 20) and 1 g kg-1 DEHP group (n = 20). Pregnant dams in different group received respective intervention by gavage once daily from embryonic day (E)6.5 to E14.5. Maternal weights were monitored every day and samples were collected at E15.5. Hematoxylin and eosin staining was used to examine fetal cardiac malformations. Real-time quantitative polymerase chain reaction and western blot were applied to detect peroxisome proliferator-activated receptor (PPAR)α/PPARγ/Nkx2.5/Gata4/Tbx5/Mef2c/Chf1 mRNA and protein expression, respectively. Maternal DEHP exposure significantly decreased maternal body weight, fetal weight and placental weight, and remarkably elevated fetal cardiac malformations rate. The phenotypes of cardiac anomalies mainly include septal defects, ventricular myocardium noncompaction and cardiac hypoplasia. Higher doses DEHP (500 mg kg-1 and 1 g kg-1 ) could significantly decreased fetal cardiac Gata4/Mef2c/Chf1 expression, while PPARγ expression was upregulated. Maternal exposure to higher doses of DEHP could result in fetal cardiac development malformations in mice and it might have resulted from the inhibition of cardiac GATA4/Mef2c/Chf1 expression via PPARγ activation.
Keywords
Environmental Studies--Toxicology And Environmental Safety; cardiac development; di‐(2‐ethylhexyl)‐phthalate; Heart diseases; Peroxisome proliferator-activated receptors; Polymerase chain reaction; Hypoplasia; Exposure; Fuel consumption; Rodents; Myocardium; Heart rate; Body weight; Fetuses; Corn oil; Embryos; Abnormalities; Gene expression; Nkx2.5 protein; Ventricle; Placenta
Tags
IRIS
•
Dibutyl Phthalate (DBP)
Database Searches
LitSearch July 2017 - Sept 2018
New from Previous
Pubmed
•
Phthalates – Targeted Search for Epidemiological Studies
Source - August 2018 Update
Pubmed
Toxline
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