Mycotoxin Zearalenone induced apoptosis in BEAS-2B cells through generation of ROS and activation of JNK and p38 MAPKs signalling pathways

Abstract

Human exposure to Zearalenone (ZEA, a non-steroidal estrogenic mycotoxin) through inhalation has raised considerable concern. However, the potential health risk and the mechanism of actions of ZEA are not well understood. In the present study, we used BEAS-2B, cultured human bronchial epithelial cells, as well as Cygb stably transfected BEAS-2B cells to study the cytotoxic effects and the toxic mechanisms of ZEA. Our results indicated that ZEA decreased cell viability, induced apoptosis and promoted ROS level in BEAS-2B cells. Oxidative stress was clearly evident, as shown by an elevated mRNA expression levels of oxidative stress markers (Hsp70 and Hsp27) and endogenous antioxidants (SOD2 and Gpx). Stable transfection of Cygb significantly increased the level of Cygb but reduced level of ROS and the percentage of apoptotic cells induced by ZEA. Cells pretreated with either p38 or JNK inhibitors showed no attenuation in ROS level, but the percentage of apoptotic cells was lower than cells treated with ZEA