Nitenpyram-Induced Cardiac Toxicity in Early Developmental Stages of Zebrafish.

Abstract

Nitenpyram is a new neonicotinoid insecticide primarily used for the control of piercing-sucking pests as well as fleas and lice on animals. It is widely used around the world, and the concentrations and detection rates in surface water and groundwater are increasing. Current research has shown that nitenpyram is toxic to honey bee, silkworms, and other organisms, but the toxicity to aquatic organisms and the mechanisms of its toxicity are still unclear. This study uses zebrafish as the research model to investigate the adverse effects of nitenpyram on the early embryonic development of zebrafish. The results show that nitenpyram induces developmental toxicity and cardiac toxicity in zebrafish. Zebrafish exhibited pericardial edema and an increased distance between the atria and ventricles. Quantitative real-time PCR (qRT-PCR) analysis revealed that the expression of heart development-related genes tbx2b, gata4, vmhc, myh6, and nkx2.5 was inhibited. Additionally, nitenpyram induced oxidative stress in zebrafish, significantly increasing the production and accumulation of ROS in the cardiac region. Acridine orange staining results revealed that nitenpyram induced apoptosis in the cardiac region of zebrafish, and qRT-PCR results showed activation of the endogenous apoptosis pathways. Therefore, it is speculated that nitenpyram-induced oxidative stress alters the expression of heart-related genes and triggers endogenous apoptosis in zebrafish cardiomyocytes, ultimately leading to abnormal cardiac development.