Deoxynivalenol induces apoptosis in mouse thymic epithelial cells through mitochondria-mediated pathway

• Deoxynivalenol (DON) can induce apoptosis in mouse thymic epithelial cell line 1 (MTEC1).
• DON can increase the protein levels of p53 in MTEC1 cells.
• DON can increase reactive oxygen species levels and decrease mitochondrial membrane potential in MTEC1 cells.
• DON can increase the expression levels of apoptosis-associated proteins in MTEC1 cells.

Deoxynivalenol (DON) is a mycotoxin produced as a secondary metabolite by fungal species. In this report, we investigated the apoptotic effect of DON in mouse thymic epithelial cell line 1 (MTEC1). MTEC1 cell apoptosis induced by DON was confirmed by nuclei morphology change, TUNEL positive staining, annexin V/propidium iodide positive staining and increased protein levels of caspase-3, caspase-8, caspase-9 and poly(ADP-ribose) polymerase (PARP). The effects of DON on reactive oxygen species (ROS) levels and mitochondrial membrane potential were investigated via fluorescence microscope and flow cytometry, respectively. In addition, DON could significantly increase the protein levels of p53 and Bax/Bcl-2 ratio in MTEC1 cells. Taken together, our results suggest that DON causes the activation of p53, increased levels of ROS and the induction of mitochondrial dysfunction, which may contribute to DON-induced apoptosis in MTEC1 cells.