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Thirty Weeks of Microplastics Exposure Alters Muscle Quality in Grass Carp ( Ctenopharyngodon idella ) Revealed by Transcriptomics and Metabolomics
Summary
Scientists exposed grass carp (a common food fish) to microplastics for 30 weeks and found that it altered hundreds of genes and chemical processes in the fish's muscle—the part we actually eat—leading to signs of stress, inflammation, and changes in tissue structure. Since microplastics are already widespread in rivers, lakes, and fish farms, this research suggests that long-term exposure could affect the quality and safety of fish on our plates, though more research is needed to understand what this means for people who eat them.
Microplastics (MPs) are tiny particles with a diameter of less than 5 mm generated from the breakdown of plastic waste. In recent years, MPs have extensively entered aquatic environments and accumulated in fish tissues, including the intestine, liver, kidney, and muscle. Previous studies have demonstrated that MP exposure can damage fish organs such as the gastrointestinal tract, gills, and liver, and may pose potential health risks to humans through the food chain. However, the toxicological effects of long-term MP exposure on the muscle tissue of grass carp (Ctenopharyngodon idella), an important edible fish species, remain poorly understood. In this study, we employed an integrated transcriptomic and metabolomic approach to investigate the molecular pathways and metabolic processes in grass carp muscle under 30-week long-term MP exposure. At the transcriptomic level, a total of 1549 genes were upregulated, whereas 1777 genes were downregulated. Gene Ontology (GO) enrichment analysis revealed that 66.6% of differentially expressed genes (DEGs) were assigned to cellular components (CC), with the extracellular space and extracellular region being the most significantly enriched terms. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that ECM-receptor interaction, focal adhesion, and PI3K-Akt signaling pathways were significantly affected. At the metabolomic level, 118 metabolites were significantly upregulated, whereas 132 metabolites were significantly downregulated, with heterocyclic compounds, alcohols, and amines being notably decreased. KEGG enrichment analysis revealed that these differential metabolites were primarily involved in ABC transporters, sphingolipid metabolism, and d-amino acid metabolism pathways. Integrated analysis suggested that long-term MP exposure induces ECM remodeling and membrane lipid metabolism abnormalities by modulating ECM-related genes and signaling pathways, and may compromise fish muscle quality through mechanisms involving oxidative stress and inflammatory responses. Overall, this study provides novel evidence for the toxicological effects and molecular mechanisms underlying long-term MP exposure and offers important insights for sustainable aquaculture practices and food safety risk assessment.