Evaluation of deoxynivalenol-induced toxic effects on DF-1 cells in vitro: Cell-cycle arrest, oxidative stress, and apoptosis

• Deoxynivalenol (DON) can decrease cell viability in DF-1 cells.
• DON can inhibit the proliferation of DF-1 cells through G2/M phase arrest in the cell cycle progression.
• DON can induce oxidative stress in DF-1 cells.
• DON can cause mitochondria damage and apoptosis in DF-1 cells.

Deoxynivalenol (DON) is one of the most common mycotoxin contaminants of raw and processed cereal food. Lymphoid cells and fibroblasts are specified to be the most DON-sensitive cell types. In this study, we investigated the toxic effects of DON in chicken embryo fibroblast DF-1 cells. The results showed that DON significantly inhibited DF-1 cell viability in both a time- and concentration-dependent manner. DON could also inhibit the proliferation of DF-1 cells through G2/M phase arrest in the cell cycle progression. Moreover, oxidative stress induced by DON was indicated by increased levels of reactive oxygen species (ROS), malondialdehyde (MDA), and decreased levels of glutathione (GSH) and superoxide dismutase (SOD). In addition, DON could also cause mitochondrial damage by decreasing the mitochondrial membrane potential and induce apoptosis accompanied with the up-regulation of apoptosis-related genes including Caspase-3, Caspase-8, Caspase-9, and AIFM1. These results suggested that DON could cause cell cycle arrest, oxidative stress, and apoptosis in DF-1 cells.