Neurotoxicity Assessment of Amicarbazone Using Larval Zebrafish

Amicarbazone (AMZ), a triazolinone herbicide widely applied in agriculture, is known to inhibit photosystem II in target plants, disrupting photosynthesis and causing oxidative stress that leads to weed mortality. Despite its widespread use, the developmental and neurotoxic effects of AMZ on aquatic organisms remain underexplored. This study assesses the impact of AMZ exposure on zebrafish (<i>Danio rerio</i>) embryos/larvae, focusing on developmental toxicity and neurotoxicity. Zebrafish were exposed to AMZ at various concentrations to evaluate survival, malformations, heart rate, and behavior. Significant developmental defects, including reduced survival rates, increased malformations, and decreased heart rates, were observed in zebrafish embryos exposed to AMZ, particularly at higher concentrations. Additionally, behavioral assays revealed decreased locomotor activity, particularly at concentrations of 100 and 200 mg/L. Moreover, AMZ exposure disrupted motor axon formation, oligodendrocyte development, and the expression of key genes involved in neurodevelopment. The downregulation of cholinergic, dopaminergic, and serotonergic signaling pathways was also identified, indicating neurotoxicity. These findings highlight AMZ's potential to induce both developmental and neurotoxic effects in zebrafish and suggest the need for further research on its long-term ecological impacts.