Mevinphos induces developmental defects via inflammation, apoptosis, and altered MAPK and Akt signaling pathways in zebrafish

Abstract

Mevinphos, an organophosphate insecticide, is widely used to control pests and enhance crop yield. Because of its high solubility, it can easily flow into water and threaten the aquatic environment, and it is known to be hazardous to non-target organisms. However, little is known about its developmental toxicity and the underlying toxic mechanisms. In this study, we utilized zebrafish, which is frequently used for toxicological research to estimate the toxicity in other aquatic organisms or vertebrates including humans, to elucidate the developmental defects induced by mevinphos. Here, we observed that mevinphos induced various phenotypical abnormalities, such as diminished eyes and head sizes, shortened body length, loss of swim bladder, and increased pericardiac edema. Also, exposure to mevinphos triggered inflammation, apoptosis, and DNA fragmentation in zebrafish larvae. In addition, MAPK and Akt signaling pathways, which control apoptosis, inflammation, and proper development of various organs, were also altered by the treatment of mevinphos. Furthermore, these factors induced various organ defects which were confirmed by various transgenic models. We identified neuronal toxicity through transgenic olig2:dsRed zebrafish, cardiovascular toxicity through transgenic fli1:eGFP zebrafish, and hepatotoxicity and pancreatic toxicity through transgenic lfabp:dsRed;elastase:GFP zebrafish. Overall, our results elucidated the developmental toxicities of mevinphos in zebrafish and provided the parameters for the assessment of toxicities in aquatic environments.