Atrazine exposure induces necroptosis through the P450/ROS pathway and causes inflammation in the gill of common carp (Cyprinus carpioL.)

Abstract

Atrazine (ATR) is used worldwide and has been confirmed be hazardous materials that harmful to the health of organisms. Since ATR was more persistent in the water, the specific damage caused by ATR to aquatic organisms should be concern. The role of P450/ROS has been proposed in many pathomechanisms. To explore whether P450/ROS mediated necroptosis and promote inflammatory response caused by ATR exposure, 120 common carp (Cyprinus carpio L.) were randomly divided into four groups which were exposed to 0 μg/L, 4 μg/L, 40 μg/L and 400 μg/L ATR respectively. The residual levels of ATR and its metabolites increased, signs of necrosis and inflammation were found in the gills of the ATR-treatment groups. The levels of ROS and cytochrome P450 content were increased, and P450 enzymes were activated. The expression levels of the core components of necroptosis (RIPK1, RIPK3 and MLKL) increased. Moreover, gene expression of inflammatory factors (TNF-α, NF-κB, iNOS, COX-2, IL-1β and PTGE) increased significantly in the ATR-spiked group. Our results suggested that ATR exposure triggered necroptosis through the P450/ROS pathway and causes inflammation of common carp gill. This study provides valuable clue about the mechanism by which ATR causes injury to common carp gill.