Atrazine exposure triggers common carp neutrophil apoptosis via the CYP450s/ROS pathway

Due to the excessive pursuit of crop yields and the abuse of herbicides, water pollution caused by atrazine (ATR) has become one of the most severe environmental issues threatening the health of fish and aquatic animals. However, no detailed report has been conducted on the mechanisms of ATR immunotoxicity in fish neutrophils. To investigate these mechanism, we exposed peripheral blood neutrophils to 25 μg/ml atrazine for 1, 2, and 3 h. The results showed that ATR induced the mRNA expression of CYPs enzymes (CYP1A1, CYP1B1, CYP1C and CYP3A138), which increased the ROS levels, and inhibited the SOD and CAT activities, GSH content and spurred the accumulation of MDA. Additionally, a significant decline in the OXPHOS, Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase activities of mitochondria was observed after ATR exposure. Concurrently, ATR activated Caspase3 and induced apoptosis by changing the expression of mitochondrial pathway factors (Bcl-2, BAX, Caspase9) and death receptor pathway major genes (TNF-α, TNFR, Fas, FasL, and Caspase8). The results reported here indicate that the oxidative stress and mitochondrial damage caused by ATR metabolism may play a crucial role in the apoptosis of carp neutrophils, and enrich the immunotoxicological mechanisms of ATR observed in fish.