Folate antagonism following teratogenic exposure to diphenylhydantoin.
Previous studies have reported indirect evidence for the mediation of folate antagonism in the induction of malformations by diphenylhydantion. We have demonstrated that a teratogenic regimen of folate-deficiency and antagonism using 9-methyl PGA in the rat produces significantly decreased rates of oxygen consumption in the maldeveloping embryos. The present study reports similar reductions in oxygen uptake by mouse embryos from mothers treated with teratogenic doses of diphenylhydantoin, and documents a significant depression of the actual folate levels in such embryos. The differences are less significant with lower doses of diphenylhydantoin, and do not occur with a nonteratogenic dose.
D000014:Abnormalities, Drug-Induced / Q000209:etiology*; D000818:Animals; D005260:Female; D005327:Fetal Resorption / Q000139:chemically induced; D005333:Fetus / Q000378:metabolism; D005493:Folic Acid Antagonists / Q000633:toxicity*; D005494:Folic Acid Deficiency / Q000139:chemically induced*; D008297:Male; D051379:Mice; D010101:Oxygen Consumption / Q000187:drug effects; D010672:Phenytoin / Q000633:toxicity*; D011247:Pregnancy
D005493:Folic Acid Antagonists; D010672:Phenytoin