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Co-exposure to triclosan and polystyrene nanoplastics on neurodevelopmental toxicity and gut microbiota dysbiosis in zebrafish (Danio rerio)
Summary
Researchers investigated the combined effects of triclosan and polystyrene nanoplastics on zebrafish development and found that co-exposure worsened neurodevelopmental toxicity beyond the effects of either pollutant alone. The combined exposure caused significant gut microbiota disruption and altered expression of genes involved in neural development, suggesting synergistic toxic effects between these two common environmental contaminants.
Triclosan (TCS) and nanoplastics (NPs) are emerging environmental pollutants frequently found in human-related samples. While prior research has investigated TCS's neuro and enterotoxicity, the combined effects of TCS and NPs remain unclear. The polystyrene nanoplastics (PS-NPs, 100 nm) were characterized by scanning electron microscopy (SEM) and nanoparticle tracking analysis, and the interaction and physical properties of polystyrene nanoplastic and TCS under co-exposure were characterized by Fourier transform infrared spectroscopy and SEM. We conducted acute exposure (6 hpf-5 dpf) and chronic exposure (6 hpf-90 dpf) experiments on zebrafish larvae, that is, co-exposure to TCS (250 μg/L) and PS-NPs (100 μg/L, 1000 μg/L). The distribution characteristics of PS-NPs and TCS + PS-NPs in vivo were studied using fluorescent PS-NPs. In addition, the results were evaluated by histopathology, behavioral tests, 16S rDNA sequencing and comparative toxicogenomic database analysis (CTD). In the co-exposure to TCS and PS-NPs, TCS did not alter the distribution characteristics of PS-NPs in zebrafish larvae. The co-exposure exacerbated neurodevelopmental inhibition, leading to neurodevelopmental abnormalities in zebrafish larvae, including developmental malformations, reduced spontaneous motor activity. Additionally, significant behavioral abnormalities were observed in adult zebrafish, such as reduced motor activity and delayed responses. Analysis of the CTD database suggested that the oxidative stress response pathway might mediate the neurotoxicity and gut microbiota dysbiosis caused by TCS + PS-NPs, with a focus on changes in neurodevelopmental genes (syn2a, ngn1, gap-43). Chronic co-exposure resulted in dysbiosis and decreased diversity of the gut microbiota in adult zebrafish, as well as various histopathological damages, such as partial shedding of intestinal villi and thinning of the intestinal wall. In general, the co-exposure of TCS and PS-NPs exacerbates the oxidative stress response and further induces neurodevelopmental toxicity and intestinal microbiota dysregulation. The assessment of the complex interaction between the two reveals the environmental risks of emerging pollutants and nanoplastics coexisting.
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