Bifenazate exposure induces cardiotoxicity in zebrafish embryos

Bifenazate is a novel acaricide for selective foliar spraying and is widely used to control mites in agricultural production. However, its toxicity to aquatic organisms is unknown. Here, a zebrafish model was used to study bifenazate toxicity to aquatic organisms. Exposure to bifenazate was found to cause severe cardiotoxicity in zebrafish embryos, along with disorders in the gene expression related to heart development. Bifenazate also caused oxidative stress. Cardiotoxicity caused by bifenazate was partially rescued by astaxanthin (an antioxidant), accompanied by cardiac genes and oxidative stress-related indicators becoming normalized. Our results showed that exposure to bifenazate can significantly change the ATPase activity and gene expression levels of the calcium signaling pathway. These led to heart failure, in which the blood accumulated outside the heart without entering it, eventually leading to death. The results indicated that bifenazate exposure caused cardiotoxicity in zebrafish embryos through the induction of oxidative stress and inhibition of the calcium signaling pathway. (C) 2021 Elsevier Ltd. All rights reserved.

Automated summary

The study showed that bifenazate exposure has significant toxicity to aquatic organisms, especially zebrafish. Exposure to bifenazate causes severe cardiac toxicity in zebrafish, which can be partially alleviated by the antioxidant astaxanthin, indicating oxidative stress as a key mechanism in bifenazate-induced cardiotoxicity.