Dicamba has been used worldwide for 60 years, but few studies have been conducted on its environmental safety and health effects. Therefore, this study aims to evaluate the acute toxicity, teratogenic effects, oxidative stress, and neurotoxicity of Dicamba in zebrafish embryos. Embryos were exposed to concentrations of 4.5, 18, 72, and 288 mg/L of Dicamba for 96 h. Among the teratogenic effects, yolk sac edema predominated, besides malabsorption of nutrients (grayish yolk sac). The presence of edema may indicate problems with circulation and water efflux from the embryos, which may be related to kidney and cardiovascular problems. Other effects such as hemorrhage, spinal and eye malformations, and dwarfism were also observed. The hatching rate was reduced in the highest concentration, and in the other concentrations, a decrease was noticeable indicating a delay in development. Neurotoxic effects were also observed. Oxidative stress analysis showed a significant decrease in SOD at all concentrations and an increase in GPx, GSH, and LPO at 288 mg/L of Dicamba. It was observed that the herbicide is capable of causing teratogenic effects, developmental delay, and oxidative stress. These results show that exposure to Dicamba, in a commercial formulation, can bring risks during embryonic development. In addition, it highlights the need for further studies on the effects of the herbicide and a reassessment of toxicity categorization.
Keywords: Acetylcholinesterase; Acute toxicity; Malformations; Oxidative stress; Pesticides.
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