Maternal fumonisin exposure as a risk factor for neural tube defects.

摘要: Abstract Fumonisins are mycotoxins produced by the fungus F. verticillioides, a common contaminant of maize (corn) worldwide. Maternal consumption fumonisin B1‐contaminated during early pregnancy has recently been associated with increased risk for neural tube defects (NTDs) in human populations that rely heavily on as dietary staple. Experimental administration purified to mice gestation also results an incidence NTDs exposed offspring. Fumonisin inhibits enzyme ceramide synthase de novo sphingolipid biosynthesis, resulting elevation free sphingoid bases and depletion downstream glycosphingolipids. Increased base metabolites (i.e., sphinganine‐1‐phosphate) may perturb signaling cascades involved embryonic morphogenesis functioning ligands sphingosine‐1‐P (S1P) receptors, family G‐protein‐coupled receptors regulate key biological processes such cell survival/proliferation, differentiation migration. Fumonisin‐induced glycosphingolipids impairs expression function GPI‐anchored folate receptor (Folr1), which contribute adverse outcomes. appear be multifactorial origin, involving complex gene‐nutrient‐environment interactions. Vitamin supplements containing folic acid have shown reduce occurrence NTDs, help protect developing fetus from environmental teratogens. factor birth defects, although other aspects maternal nutrition genetics play interactive roles determining outcome. Minimizing exposures through enhanced agricultural practices, identifying biomarkers exposure, characterizing mechanisms toxicity, improving all important strategies reducing NTD burden susceptible populations.