Chronic Exposure of Adult Zebrafish to Polyethylene and Polyester-based Microplastics: Metabolomic and Gut Microbiome...

The study explored the ecotoxicological effects of chronic exposure to microplastic (MP) on adult zebrafish, focusing on environmentally relevant concentrations of polyethylene (PE) beads and polyester (PES). High-throughput untargeted metabolomics via UPLC-QToF-MS and 16S metagenomics for gut microbiota analysis were used to assess ecotoxicity in zebrafish exposed to varying concentrations of PE and PES. The VIP (Variable Importance in Projection) scores indicated PE exposure primarily impacted phospholipids, ceramides, and nucleotide-related compounds, while PES exposure led to alterations in lipid-related compounds, chitin, and amino acid derivatives. From MSEA (Metabolite Set Enrichment Analysis) and Mummichog analyses, PE and PES significantly disrupted key metabolomic pathways associated with inflammation, immune responses, and apoptosis, including leukotriene and arachidonic acid metabolism and the formation of putative anti-inflammatory metabolites from EPA. PE caused physical disruption and inflammation of the epithelial barrier, whereas PES affected gut microbiota interactions, impairing digestion and metabolism. Although alpha diversity within the gut microbiome remained stable, beta diversity analysis revealed significant shifts in microbial composition and structure, suggesting a disruption of functional balance and an increased susceptibility to pathogens. Chronic PE and PES exposures induced shifts in the gut microbial community and interaction network with potential increases in pathogenic bacteria and alteration in commensal bacteria, demonstrating the microbiome's resilience and adaptability to stressors of MPs exposure. High-throughput metabolomics and 16S metagenomics revealed potential chronic diseases associated with inflammation, immune system disorders, metabolic dysfunction, and gut dysbiosis, highlighting the complex relationship between gut microbiome resilience and metabolic disruption under MP-induced stress, with significant ecological implications.