Document Detail

Ethanol-induced inhibition of fetal hypothalamic-pituitary-adrenal axis due to prenatal overexposure to maternal glucocorticoid in mice.
MedLine Citation:
PMID:  20627497     Owner:  NLM     Status:  In-Data-Review    
Prenatal ethanol exposure has been well documented to be one of the etiological factors responsible for intrauterine growth retardation (IUGR). Previous studies have shown that chronic ethanol exposure during pregnancy elevated the basic level of corticosterone in fetus. However, the potential mechanisms behind them are still unclear. The aim of the present study was to investigate the effects of prenatal ethanol exposure on maternal and fetal hypothalamic-pituitary-adrenal (HPA) axis as well as placental 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), and to clarify the mechanism of ethanol-induced IUGR. Pregnant mice were intragastricly administrated with ethanol at a dose of 6.4gkg(-1)d(-1) from day 11 to 17 of gestation and parameters representing fetal growth and development were recorded either. The level of corticosterone in maternal serum was determined by ELISA kit. The mRNA expressions of steroidogenic acute regulatory protein (StAR) and cytochrome P450 cholesterol side chain cleavage (P450scc) both in maternal and fetal adrenal, and placental 11β-HSD-2 were detected by real-time quantitative PCR, respectively. The results showed that fetal body weight significantly decreased, and the incidence of IUGR was obviously increased after prenatal ethanol exposure. Maternal serum corticosterone level was elevated, and the expressions of StAR and P450scc were increased in maternal adrenal while decreased in fetal adrenal. The expression of placental 11β-HSD-2 was significantly reduced. These results suggest that prenatal ethanol exposure induces an inhibition of fetal HPA axis activity and IUGR occurs. The mechanism may be associated with ethanol-induced maternal HPA axis activation and high glucocorticoid condition, which impair the placental barrier, and lead to an overexposure of elevated maternal glucocorticoid to fetus, and eventually result in the inhibition of the fetal HPA axis.
Gai Liang; Man Chen; Xiao-Liang Pan; Jiang Zheng; Hui Wang
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Publication Detail:
Type:  Journal Article     Date:  2010-06-07
Journal Detail:
Title:  Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie     Volume:  63     ISSN:  1618-1433     ISO Abbreviation:  Exp. Toxicol. Pathol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-09-29     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9208920     Medline TA:  Exp Toxicol Pathol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  607-11     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier GmbH. All rights reserved.
Pharmacology Department of Basic Medical College, Wuhan University, Wuhan 430071, China.
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