Curcumin attenuates beauvericin-induced global DNA methylation alterations in liver and colon cells.

Beauvericin (BEA) is an emerging mycotoxin with various reported toxic effects. Since BEA is considered non-genotoxic, epigenetic mechanisms may contribute to its toxicity. This study investigated the effects of BEA on global DNA methylation (5-mC) and hydroxymethylation (5-hmC), the expression of genes involved in these processes, and the modulatory potential of curcumin (CUR). After 24 h of BEA exposure, the IC50 values were 15.93 μM in HepG2 cells and 16.57 μM in HCT116 cells, decreasing to 0.98 μM and 0.30 μM after 48 h. Co-treatment with 5 μM CUR significantly restored cell viability. BEA significantly decreased 5-mC levels and increased 5-hmC levels in both cell lines. CUR modulated 5-mC levels and BEA-induced 5-hmC alterations in a cell type-specific manner, enhancing 5-hmC in HepG2 cells while reducing it in HCT116 cells. BEA and CUR also altered the expression of genes involved in DNA methylation and hydroxymethylation. Docking analysis suggested interactions of BEA and CUR with proteins involved in these pathways. These findings provide insight into BEA toxicity mechanisms and the modulatory effects of CUR through integrated in vitro and in silico analyses.