Fipronil has been widely used in agriculture to prevent aggressive insects from damaging agricultural products. Fipronil residues circulate in the environment and they have been detected in non-targeted organisms in aquatic environments. To study the effect of fipronil toxicity on environmental health, 6 h post fertilization (hpf) zebrafish embryos were treated with fipronil for 72 h. LC50 value was obtained by applying varying concentrations of fipronil to zebrafish embryos for 72 h. As zebrafish embryos are useful vertebrate models for studying developmental and genetic findings in toxicology research, they were exposed to fipronil to study detailed elucidating mechanisms with hazardous end points of toxicity. Cell cycle arrest-related apoptosis supported pathological alterations, such as increased mortality, shortened body length, and reduced hatchability. Furthermore, observed heart defects, including edema and irregular heartbeat were caused due to abnormal blood circulation. In transgenic zebrafish models (fli1:eGFP and olig2:dsRED), disrupted blood vessel formations were indicated by eGFP+ endothelial cells. Moreover, neurogenic defects were observed by studying dsRED+ motor neurons and oligodendrocytes. This study demonstrates fipronil accumulation in aquatic environment and its ability to impair essential processes, such as angiogenesis and neurogenesis during early developmental stage of zebrafish, along with general developmental toxicity.
Keywords: Cardiac failure; Developmental toxicity; Embryogenesis; Fipronil; Neuronal defect.
Copyright © 2019 Elsevier B.V. All rights reserved.