Hepatic toxicity assessment of organophosphorus insecticide isazophos on zebrafish

Abstract

Isazophos, an organophosphorus insecticide, is a prevalent environmental contaminant that bioaccumulates in organisms and poses significant risks to human health. However, the organ toxicity of isazophos to aquatic organisms has not been previously characterized. The purpose of this study is to investigate the toxic effects of isazophos exposure on zabrafish liver, as well as revealing the underlying toxicological mechanisms. Acute and chronic toxicity assessments showed 72 h and 28 days lethal concentration (LC₅₀) values of 2.612 mg/L and 0.172 mg/L for zebrafish embryos and adult zebrafish, respectively. The level of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and inflammation related genes revealed that isazophos affects early zebrafish development and causes liver damage via reactive oxygen species (ROS)-induced oxidative stress and inflammatory with upregulated pro-inflammatory factors (il-6, il-8, il-1β and TNF-α). Moreover, when exposed to isazophos, the glycogen content of the liver was decreased, while lipid accumulation was increased, and liver metabolism-related indices were changed. The ratios of pro-apoptotic genes p53, bax/bcl-2, caspase 9 and caspase 3 were upregulated. And the caspase3 and cleaved-caspase3 protein expression was evaluated in the isazophos group, revealing that isazophos caused aptoptotic. In conclusion, isazophos induces oxidative stress through the production of ROS, leading to the activation of pathways associated with apoptosis. The present study provides a systematic analysis of isazophos-induced hepatic effects in zebrafish liver and demonstrates that exposure to isazophos affects normal hepatic metabolism.