Pyrazosulfuron-Ethyl Exposure Induces Neurotoxicity and Behavior Disorders in the Early Stages of Zebrafish Life

Abstract

Pyrazosulfuron-ethyl is one of the most used herbicides in agriculture, which is a member of the sulfonylurea group of herbicides. The possible hazardous effects of pyrazosulfuron-ethyl on aquatic creatures and its probable toxicity mechanisms are still poorly known despite its expanding use. In this paper, zebrafish embryos were acutely exposed to 25 mg/L, 50 mg/L, and 100 mg/L pyrazosulfuron-ethyl solution from 6 hours post fertilization (hpf) to 24 hpf. The findings revealed that the treated embryos showed delayed yolk absorption, retarded head development, blurred ventricles, malformed eyes, dramatically reduced tail flapping frequency at 24 hpf, and developmental deformities in the tail. Moreover, following 24 hours of treatment, the motor ability of 5 dpf zebrafish larvae exposed to the same density gradient was drastically diminished. Acetylcholinesterase (AChE) activity was changed, and oxidative stress was up-regulated in zebrafish embryos after exposure to pyrazosulfuron-ethyl. At the same time, pyrazosulfuron-ethyl induced more apoptosis and affected gene expression relevant to neurodevelopment, neurotransmitter systems, and specific neural in the brain. In conclusion, pyrazosulfuron-ethyl can cause aberrant motor behavior and neurodevelopmental damage in the early stages of zebrafish life.

Keywords: Pyrazosulfuron-ethyl, Neurotoxicity, Oxidative stress, RA signaling, zebrafish