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.