Exposure to the herbicide fluridone induces cardiovascular toxicity in early developmental stages of zebrafish

Abstract

Fluridone is a systemic herbicide used to control a range of invasive aquatic plants in irrigation systems, lake, and reservoirs. Since aquatic herbicides are more likely to have a hazardous impact on ecosystems than terrestrially applied herbicides, a risk assessment is needed to determine whether to expand or limit their use. The aim of this study was to investigate the developmental toxicity of fluridone using zebrafish. Diverse toxicological results were observed for the sub-lethal endpoints, including lack of hatching, reduced heartbeat and disturbed blood circulation through dysmorphic heart, and edema formation. Abnormal apoptosis was observed in the brain and yolk sac of fluridone-exposed larvae. A computational analysis was used to predict chemical properties in non-target organisms and revealed that fluridone was highly relevant in the cardiovascular system. Double transgenic zebrafish (fli1a:EGFP;cmlc2:dsRed) were used to evaluate the effects of fluridone on the cardiovascular system during embryonic development. Ectopic growth of sub-intestinal vessels and sprouting angiogenesis in the hindbrain region were highly inhibited. Additionally, essential genes involved in the VEGF signaling and heart development were differentially expressed in dose-dependent manner. Collectively, our toxicological findings in fluridone exposure highlight defects in the cardiovascular development causing embryonic lethality that could damage aquatic communities and natural ecosystems.

Keywords: Apoptosis; Cardiovascular toxicity; Fluridone; Gene expression; Zebrafish embryos.