Cell-type specific effects of Fusarium mycotoxins on primary neuronal and astroglial cells

Fumonisin B1, deoxynivalenol (DON) and zearalenone (ZEA) are toxic secondary metabolites produced by Fusarium molds. These mycotoxins are common food and feed pollutants and represent a risk for human and animal health. Although the mycotoxins produced by this genus can cross the blood-brain-barrier (BBB) in many species, their effect on neuronal function remains unclear. We investigated cell viability effects of these toxins on specified neural cell types, including mouse primary neuronal, astroglial and mixed cell cultures 24 or 48 hours after mycotoxin administration. Cell viability assay revealed that DON decreased cell viability in a dose-dependent manner, independently from the cultures type. Fumonisin B1 increased cell viability significantly on astroglial and mixed cell cultures in lower doses, while it exerted a highly toxic effect in 50 {micro}M. ZEA had significant effects on all culture type in 10 nM by increasing the cell viability. Since ZEA is a mycoestrogen, we analyzed the effects of ZEA on the expression of estrogen receptor isotypes ER and ER{beta} and mitochondrial voltage-dependent anion channel (VDAC1) by qRT-PCR. In neuronal and mixed cultures, ZEA administration decreased ER expression, while in astroglial cultures, it induced the opposite effect. ER{beta} and VDAC1 expression was not altered by ZEA in either culture types. ZEA also affected the firing pattern of neurons by enhancing the burst frequency. Our results demonstrate that Fusarium mycotoxins are acting on a cell specific manner in the brain tissue.