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Microplastic exposure induces structural hyperplasia in the gill tissue of grass carp (Ctenopharyngodon idellus) through immunosuppression, metabolic disruption, and structural damage
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Researchers examined how polystyrene microplastics affect the gill tissue of grass carp at two concentrations. They found that higher microplastic exposure caused significant structural damage to gills, activated inflammatory pathways, triggered oxidative stress, and promoted abnormal cell proliferation. The study suggests that microplastics can induce structural hyperplasia in fish gills through combined immunosuppression, metabolic disruption, and tissue damage mechanisms.
Microplastics (MPs), as ubiquitous pollutants in aquatic environments, constitute a significant component of water pollution, posing substantial ingestion risks to directly exposed fish. However, research on the potential toxic effects and underlying mechanisms of MPs on fish gills remains insufficient. Therefore, this study investigated the impacts of exposure to different concentrations of polystyrene MPs (100 and 400 μg/L) on the histological structure and gene expression in the gills of grass carp (Ctenopharyngodon idellus). Through integrated histopathological and transcriptomic analyses, we systematically evaluated the effects of MPs exposure. Results showed that the 400 μg/L MPs group exhibited significantly higher gill structural damage compared to the 100 μg/L group, alongside more severe cellular apoptosis. The results of the transcriptome analysis reveal that microplastic exposure induces pathological changes in the gill filament epithelial cells, activates complement and coagulation cascade reactions, as well as the JAK-STAT pathway, promoting inflammatory damage and cell proliferation. Concurrently, MPs exposure activated the NF-κB pathway, triggered oxidative stress responses, and elicited gill inflammation via the Cell Adhesion Molecules (CAMs) and TNF signaling pathways. Furthermore, MPs disrupted gill redox homeostasis and activated apoptotic mechanisms, leading to structural damage and degeneration of gill tissue. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses further confirmed that MPs exposure activated multiple critical biological pathways, including cell cycle regulation, immune defense, oxidative stress, metabolism, and cellular structure. In summary, this study demonstrates that exposure to different concentrations of MPs causes structural damage, metabolic disruption, and cellular dysfunction in the gills of grass carp, indicating the high sensitivity of this direct water-contact organ to MPs pollution. This research provides important scientific foundations for understanding the ecotoxicological impacts of MPs exposure on aquaculture species.
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