Abstract
Fumonisins are fungal toxins found in maize and maize-based foods. Fumonisins are toxic to animals but their impact on human health is uncertain. Epidemiological evidence suggests that fumonisins are potential risk factors for neural tube defects (NTDs) and for growth retardation of young children living in areas where large amounts of fumonisin-contaminated corn are consumed on a regular basis. Fumonisin B1 (FB1), the most common fumonisin, was not teratogenic in some animal studies although adverse embryonic and fetal affects secondary to maternal toxicity were found. These included generalized growth impairment and, at high doses, fetal death in utero. Other investigations have, in contrast, shown that FB1 induces NTDs in some mouse strains. The etiology of NTDs is complex and involves interactions between environmental, nutritional, and genetic factors. Reasons underlying differences in the sensitivity of mouse strains to NTD induction by fumonisins are not fully understood although they likely involve fumonisin-dependent disruption of sphingolipid biosynthesis and sphingolipid-dependent effects on folate utilization and uptake, diverse cell signaling pathways, and histone modifications.