Abstract

The prevalence of microplastics (MPs), especially aged particles, interacting with contaminants like triclosan (TCS), raises concerns about their toxicological effects on aquatic life. This study focused on the impact of aged polyamide (APA) MPs and TCS on zebrafish lipid metabolism. APA MPs, with rougher surfaces and lower hydrophobicity, exhibited reduced TCS adsorption than unaged polyamide (PA) MPs. Co-exposure to PA/APA MPs and TCS resulted in higher TCS accumulation in zebrafish larvae, notably more with PA than APA. Larvae exposed to PA + TCS exhibited greater oxidative stress, disrupted lipid metabolism, and altered insulin pathway genes than those exposed to TCS. However, these negative effects were lessened in the APA + TCS group. Through miRNA-seq and miR-217 microinjection, it was revealed that PA + TCS co-exposure upregulated miR-217, linked to lipid metabolic disorders in zebrafish. Moreover, molecular docking showed stable interactions formed between PA, TCS, and the insulin signaling protein Pik3r2. This study demonstrated that PA and TCS co-exposure significantly inhibited the insulin signaling in zebrafish, triggering lipid metabolism dysregulation mediated by miR-217 upregulation, while APA and TCS co-exposure alleviated these disruptions. This research underscored the ecological and toxicological risks of aged MPs and pollutants in aquatic environments, providing crucial insights into the wider implications of MPs pollution.

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