Tralomethrin exposure disrupts neurodevelopment and locomotor function in zebrafish

Tralomethrin, an insecticide belonging to the synthetic pyrethroid class that is commonly employed in agricultural and public health applications to control pests, poses a significant risk to aquatic organisms due to its high toxicity. However, there is a notable lack of comprehensive data regarding the specific effects and mechanisms of tralomethrin toxicity in aquatic organisms. The objective of this study was to explore the toxicity of tralomethrin in zebrafish. Zebrafish embryos were exposed for 72 h to various concentrations of tralomethrin (16.63, 33.25, and 49.88 μg/L), which were selected based on preliminary experiments as non-lethal doses potentially inducing developmental malformations during early embryonic stages, a period highly sensitive to neurotoxicants. Exposure to tralomethrin leads to noticeable movement impairment, characterized by intensified twitching behavior and a noticeable increase in swimming distances. Moreover, tralomethrin exposure significantly increases acetylcholinesterase (AChE) activity and reduces fluorescence intensity in transgenic <i>Tg</i> (<i>elavl3</i>: EGFP) zebrafish. The expression patterns of genes associated with neural development, including <i>anxa5a</i>, <i>mbp</i>, <i>slc6a3</i>, and <i>th</i>, were dysregulated after tralomethrin exposure. Transcriptome sequencing analysis revealed that the differentially expressed genes (DEGs) were significantly enriched in processes related to the nervous system. Overall, these findings demonstrate that tralomethrin exposure induces neurotoxic effects in zebrafish.