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Neurodevelopmental Toxicity of Emamectin Benzoate to the Early Life Stage of Zebrafish Larvae (Danio rerio)
Summary
Researchers studied the neurodevelopmental effects of emamectin benzoate, a widely used pesticide, on zebrafish larvae at various concentrations. They found that the pesticide significantly inhibited hatching, impaired locomotor behavior, and caused neurotoxic effects including disrupted neurotransmitter levels and brain development. The study raises concerns about the ecological risks of this pesticide to aquatic organisms during their most vulnerable early life stages.
Emamectin benzoate (EMB) is a widely used pesticide and feed additive in agriculture and aquaculture. It easily enters the aquatic environment through various pathways, thus causing adverse effects on aquatic organisms. However, there are no systematic studies regarding the effects of EMB on the developmental neurotoxicity of aquatic organisms. Therefore, the aim of this study was to evaluate the neurotoxic effects and mechanisms of EMB at different concentrations (0.1, 0.25, 0.5, 1, 2, 4 and 8 μg/mL) using zebrafish as a model. The results showed that EMB significantly inhibited the hatching rate, spontaneous movement, body length, and swim bladder development of zebrafish embryos, as well as significantly increased the malformation rate of zebrafish larvae. In addition, EMB adversely affected the axon length of motor neurons in Tg (hb9: eGFP) zebrafish and central nervous system (CNS) neurons in Tg (HuC: eGFP) zebrafish and significantly inhibited the locomotor behavior of zebrafish larvae. Meanwhile, EMB induced oxidative damage and was accompanied by increasing reactive oxygen species in the brains of zebrafish larvae. In addition, gene expression involvement in oxidative stress-related (<i>cat</i>, <i>sod</i> and <i>Cu/Zn-sod</i>), GABA neural pathway-related (<i>gat1</i>, <i>gabra1</i>, <i>gad1b</i>, <i>abat</i> and <i>glsa</i>), neurodevelopmental-related (<i>syn2a</i>, <i>gfap</i>, <i>elavl3</i>, <i>shha</i>, <i>gap43</i> and <i>Nrd</i>) and swim bladder development-related (<i>foxa3</i>, <i>pbxla</i>, <i>mnx1</i>, <i>has2</i> and <i>elovlla</i>) genes was significantly affected by EMB exposure. In conclusion, our study shows that exposure to EMB during the early life stages of zebrafish significantly increases oxidative damage and inhibits early central neuronal development, motor neuron axon growth and swim bladder development, ultimately leading to neurobehavioral changes in juvenile zebrafish.
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