Quizalofop-P-ethyl induced developmental toxicity and cardiotoxicity in early life stage of zebrafish (Danio rerio)

Quizalofop-P-ethyl (QpE), a highly efficient selective herbicide, has good control effect on annual and perennial weeds. However, its excessive use will pose a threat to the ecological environment. QpE has been proven harmful to aquatic organisms, but there is little evidence on the adverse effects of QpE in the early life of aquatic or-ganisms. In this work, zebrafish (Danio rerio) embryos were treated with 0.10, 0.20, 0.30, 0.40, and 0.50 mg/L of QpE for 120 h. The findings revealed that the LC50 value of QpE to zebrafish embryos was 0.23 mg/L at 96 hpf. QpE exposure significantly increased the mortality rate, decreased the hatching rate and caused morphological defects during zebrafish embryonic development, with a concentration dependent manner. QpE also caused severe morphological changes in the cardiovascular system, as well as resulted in a dysfunction in cardiovascular performance. Meanwhile, both histopathological examination and neutrophil observations showed inflammatory response occurred in the heart. Furthermore, several genes associated with heart development and inflammation were significantly altered following QpE exposure. A protein-protein interaction (PPI) network analysis proved that there was a connection between the changed heart development-relevant and inflammation-related genes. Taken together, our findings suggest that QpE causes cardiotoxicity in zebrafish embryos by altering the expression of genes in the regulatory network of cardiac development, which might be aggravated by inflam-matory reactions, thereby affecting embryo development. These findings generated here are useful for in-depth assessment of the effects of QpE on early development of aquatic organisms and providing theoretical foundation for risk management measures.

Automated summary

Quizalofop-P-ethyl (QpE), a highly efficient selective herbicide, was found to have toxic effects on zebrafish embryos, including increased mortality rate, decreased hatching rate, morphological defects, and severe disruption in cardiovascular development. QpE exposure also led to inflammatory responses in the heart and altered the expression of genes related to heart development and inflammation, potentially affecting embryo development. These findings are important for assessing the effects of QpE on early development of aquatic organisms and designing risk management measures.