Prevention of fumonisin B1-induced neural tube defects by folic acid.
BACKGROUND
The mycotoxin fumonisin B1 (FB1) inhibits sphingolipid synthesis, blocks folate transport, and has been associated with increased incidences of cancer and neural tube defects. Results from reproductive studies in animal models in vivo and in vitro have demonstrated toxicity in some cases, but no specific terata after fumonisin exposure. No information is available about folic acid's potential to protect against this toxicity.


METHODS
Neurulating mouse embryos were exposed to fumonisin or folinic acid in whole embryo culture and assessed for effects on growth and development.


RESULTS
Fumonisin exposure inhibited sphingolipid synthesis, reduced growth, and caused cranial neural tube defects in a dose dependent manner. Supplemental folinic acid ameliorated the effects on growth and development, but not inhibition of sphingolipid synthesis.


CONCLUSIONS
Fumonisin has the potential to inhibit embryonic sphingolipid synthesis and to produce embryotoxicity and neural tube defects. Folic acid can reverse some of these effects, supporting results showing that fumonisin disrupts folate receptor function.
D000818:Animals; D004305:Dose-Response Relationship, Drug; D005492:Folic Acid / Q000494:pharmacology*; D037341:Fumonisins; D002955:Leucovorin / Q000494:pharmacology; D051379:Mice; D008855:Microscopy, Electron, Scanning; D009432:Neural Crest / Q000187:drug effects* / Q000196:embryology*; D009436:Neural Tube Defects / Q000209:etiology* / Q000517:prevention & control*; D009924:Organ Culture Techniques; D013723:Teratogens; D013997:Time Factors
D037341:Fumonisins; D013723:Teratogens; C056933:fumonisin B1; D005492:Folic Acid; D002955:Leucovorin