Paclitaxel/Cisplatin

Citalopram (CTP), a selective serotonin reuptake inhibitor, is frequently detected in aquatic environments and may reach elevated levels in effluent-impacted hotspots. This study aimed to characterize the developmental and neurobehavioral toxicity of CTP in zebrafish early life stages across an exposure gradient and to identify associated multi-level biological signatures. Zebrafish embryos/larvae were exposed to CTP (0, 0.5, 5, 50, and 500 μg/L) from 0 to 168 h post-fertilisation (hpf) under semi-static renewal to assess early-life toxicity and associated mechanistic signatures. CTP elicited non-monotonic locomotor responses, with increased activity at lower concentrations and behavioral suppression at higher concentrations. Consistent with these behavioral alterations, oxidative stress responses were biphasic: SOD activity increased significantly at lower concentrations but was suppressed at the highest concentration, while lipid peroxidation was significantly elevated under high exposure. Neurochemical analysis showed reduced 5-hydroxytryptamine and γ-aminobutyric acid at higher concentrations, co-occurring with behavioral alterations. RNA-seq at 168 hpf indicated enrichment of clock-related annotations and altered expression of selected clock-associated transcripts; rhythmicity cannot be inferred without time-series sampling. Overall, CTP induced multi-level developmental and neurobehavioral toxicity in zebrafish, accompanied by redox dysregulation and neurotransmitter perturbations. These findings highlight the value of integrating behavioral, biochemical, neurochemical, and transcriptomic endpoints for hazard characterization of neuroactive pharmaceuticals in effluent-influenced aquatic environments.