RESUMO
Pendimethalin, an herbicide used to control weeds, acts by inhibiting plant cell division and mitosis. Several studies have reported the detrimental effects of pendimethalin on non-target organisms. It has been found to be especially toxic to aquatic life. Additionally, there is some evidence that pendimethalin induces mitochondrial stress. However, none of the studies have provided information about the functional defects in mitochondria and toxicity during embryogenesis. In this study, we evaluated the impact of pendimethalin on the electron transport chain (ETC) activity and mitochondrial complexes via in vivo screening of oxidative phosphorylation and transcriptional profiles in zebrafish embryos. The results showed that pendimethalin interferes with mitochondrial complexes I and V, which inhibit embryo energy metabolism, thereby leading to developmental defects. Transgenic zebrafish, fli1:eGFP and olig2:dsRed, were used to confirm pendimethalin-induced functional depletion in neurogenesis and vasculogenesis during embryo development. This study provides new insights into the methodology of environmental assessment of biohazard chemicals that target ETC activity in mitochondria. Additionally, the results suggest that real-time respiratory and metabolic monitoring in zebrafish will be useful for the genotoxicity assessment of environmentally hazardous substances and may be used as an alternative model for the control of aquatic environmental pollutants.
