ROS acted as an initial role in selenium nanoparticles alleviating insecticide chlorpyrifos-induced oxidative stress, pyroptosis, and intestinal barrier dysfunction in porcine intestinal epithelial cells

Chlorpyrifos (CPF), a toxic organophosphorus insecticide , is widely used in agriculture to protect crops (eg., maize) from pests. The use of CPF in crops can result in accumulation in crop seeds, such as corn seeds, which is a primary feed ingredient in pigs . Pigs in China, which is an important source of animal-derived protein in the Chinese diet, account for over 50 % of the raised pig population in the whole world. Therefore, CPF may pose a potential risk to the health of non-target organisms (pigs and humans) through the food chain. However, whether CPF can damage porcine intestine remains unknown. Selenium (Se), an essential trace element , was reported to have antioxidant and anti-toxic effects. Tight junction (TJ) is an important mechanism of intestinal injury and pyroptosis is a new hotspot in the field of toxicology. Hence, we wanted to investigate whether CPF can damage pig intestine and whether selenium nanoparticles (SeNPs) supplement can alleviate CPF-induced pig intestine damage, and to study corresponding mechanism from the three aspects of OS , pytoptosis, and TJ. We established a model of SeNPs alleviating damage caused by CPF in intestinal porcine enterocytes (IPEC-J2 cells), and found that SeNPs alleviated CPF-induced oxidative stress (OS), pyroptosis , and intestinal barrier dysfunction in IPEC-J2 cells. Interestingly, OS , pyroptosis , and intestinal barrier dysfunction had serial relations, and ROS/Nrf2/Caspase-1/Occludin and ROS/Nrf2/Caspase-1/ZO-1 pathways played a role. Notably, ROS and Caspase-1 played an initial and important role, respectively. Our study added new information on pesticides-caused damage to non-target organisms, and provided new idea, insight, and targets to mitigatie pesticides-induced toxic effect on non-target organisms. • We established successfully CPF or/and SeNPs IPEC-J2 cell model. • SeNPs alleviated CPF-caused pytoptosic damage. • SeNPs alleviated CPF-induced oxidative stress, pyroptosis, and intestinal barrier dysfunction. • Oxidative stress, pyroptosis, and intestinal barrier dysfunction had serial relations on CPF or/and SeNPs treatment. • ROS acted as an initial role and Caspase-1 played an important role.