Exposure to fenvalerate causes brain impairment during zebrafish development.

Abstract Compared with increasing evidence suggesting that fenvalerate is neurotoxic to adults, further information regarding developmental toxicity of this compound attracts more attention. In this study, we used zebrafish as an environmental monitoring model to further explore the potential toxicity of fenvalerate. Our results demonstrated that larvae exposed to fenvalerate for 24–96 h displayed obvious morphological abnormalities, and the LC50 concentrations were 131.95 μg/L (LC50-24 h), 107.18 μg/L (LC50-48 h), 21.76 μg/L (LC50-72 h), and 6.25 μg/L (LC50-96 h). To further investigate the effects of fenvalerate on embryos and larvae, acridine orange staining was performed at a 50 μg/L concentration. Staining showed notable signs of apoptosis mainly in the brain. Further studies revealed that fenvalerate induced alterations in SOD activity in larvae were concentration dependent and also related to the length of exposure. Fenvalerate also down-regulated the expression of ogg1 and dlx2 genes in a concentration dependent manner, which indicated that the oxidative-DNA repair system as well as neurogenesis were impaired. In this study, we investigated the toxicity of fenvalerate using zebrafish, that provided new evidence of observable brain impairment during embryogenesis due to fenvalerate exposure and discussed their implications for the development of fenvalerate induced neurotoxicity.