Dimethoate-induced inflammation results in neurodevelopmental toxicity in zebrafish larvae

Dimethoate (DMT), a widely used organophosphorus insecticide and recognized endocrine disruptor, has emerged as a significant contaminant in aquatic ecosystems. While its environmental prevalence is well-documented, limited research exists on its neurodevelopmental toxicity in aquatic organisms. This study investigated the adverse effects of DMT exposure on zebrafish larvae, focusing on neurobehavioral impairments and underlying molecular mechanisms. Following 96-h exposure to 20 μg/L DMT, larvae exhibited marked neurodevelopmental disruptions, including reduced heart rate and diminished tail motility. Concurrently, pro-inflammatory cytokine levels (IL-8, IL-1β) were significantly elevated, suggesting systemic inflammation. Mechanistic analysis revealed dysregulation of inflammatory mediators within the TRP pathway and aberrant activation of the JAK-STAT signaling cascade. Central to these effects was the overexpression of IL-1β, which potentially drives neurotoxicity through multiple pathways: induction of apoptosis, dysregulation of neurotransmitter-associated signaling, and altered expression of genes linked to neurodegenerative disorders. These findings demonstrate that DMT compromises neurodevelopment in zebrafish larvae via IL-1β-mediated inflammatory imbalance and subsequent pathway dysregulation. This study provides critical insights into the ecotoxicological risks of DMT in aquatic environments and establishes a mechanistic framework for understanding organophosphorus-induced neurotoxicity in fish models.