Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1988-12-16
pubmed:abstractText
After a single administration of the antiepileptic drug valproic acid (VPA; i.p.:600 mg/kg) on day 8 of gestation in the mouse embryotoxicity and amniotic fluid (AF) cholinesterase (ChE) were evaluated on day 16 of gestation. VPA treatment induced an increase in embryolethality, neural tube defects (exencephaly), cleft palate, deformed vertebrae, open eyes, and a reduction in fetal weight. In VPA-exposed fetuses AF total ChE (TChE) activity of exencephalic fetuses was higher than that of normal fetuses. However, in 3 out of 110 normal fetuses of the control group TChE activity was found in the AF. There was no correlation between blood contamination of AF and its TChE activity, either in non-exencephalic control or treated embryos. Using ethopropazine as a "pseudo"-ChE inhibitor in vitro, the percentage of acetyl-ChE in blood-contaminated AF was similar to that of fetal rather than maternal serum, indicating that AF was contaminated with fetal and not with maternal blood. VPA-induced exencephaly in mice may provide an animal model to further investigate biochemical markers for prenatal diagnosis of neural tube defects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
501-3
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Amniotic fluid cholinesterase of valproate-induced exencephaly in the mouse: an animal model for prenatal diagnosis of neural tube defects.
pubmed:affiliation
Department of Pharmacology, Faculty of Pharmacy, Mansoura University, Egypt.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't