Physiological and metabolomic insights into the toxicity mechanisms of antipsychotic drug chlorpromazine hydrochloride on Microcystis aeruginosa

The antipsychotic drug chlorpromazine (CPZ) is increasingly detected in aquatic environments and has raised concerns regarding its ecological toxicity as an emerging contaminant. However, its effects on non-target aquatic organisms, particularly primary producers, remain insufficiently understood. Unlike previous studies that have mainly examined antibiotics, this is the first to comprehensively assess the multiple toxicological pathways of an antipsychotic drug in cyanobacteria. CPZ impaired photosynthesis by disrupting light energy capture, electron transport, carbon assimilation, and energy supply, as evidenced by changes in pigments (28.64% reduction in chlorophyll a content), Fv/Fm (reduced by 0.21–17.74%), and gene expression. Oxidative damage induced membrane leakage and triggered microcystin release (3.50 fold). Metabolomic analysis revealed downregulation of folate biosynthesis, suggesting reduced adaptability and functional impairment, whereas upregulation of ABC transporters indicated enhanced carbohydrate uptake and toxin efflux. These findings provide mechanistic evidence for CPZ-induced effects on Microcystis aeruginosa, which is important for its rational use and management, as well as for the establishment of water quality criteria for antipsychotic drugs. It’s also important for the understanding of potential adverse aquatic ecosystem’s consequences posed by CPZ.