LAUSR

Fumonisin B1 (FB1) is a congener of fumonisins produced by Fusarium species that may be found as corn contaminants threatening health of humans and animals. FB1 causes a variety of toxicity effects, including hepatotoxic, nephrotoxic and cytotoxic effects. However, detailed mechanisms associated with FB1 immunotoxicity in neutrophils are still unclear. To accomplish this, we utilized neutrophils to study the mechanisms of FB1 immunotoxicity. In the current study, we found that FB1 induced the formation of neutrophil extracellular traps (NETs), increased reactive oxygen species (ROS) levels, and decreased SOD and CAT activities. Concurrently, FB1 treatment led to the concentration- dependent phosphorylation of ERK-1/2 and p38 in neutrophils. Moreover, we demonstrated that FB1-induced NET formation was dependent of NADPH oxidase activity. Pretreatment of neutrophils with DPI, U0126 and SB202190 significantly reduced ROS generation, and prevented NET formation, further suggesting that ROS dependent activation of ERK 1/2 and p38 pathways, which possibly mediate FB1-induced NET release in neutrophils. Thus, NET formation and ROS production could be attributed to FB1 immunotoxicity, which might enrich the toxicological mechanisms of FB1.