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Immunotoxicity responses to polystyrene nanoplastics and their related mechanisms in the liver of zebrafish (Danio rerio) larvae
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Researchers studied how polystyrene nanoplastics affect the immune system of zebrafish larvae by examining inflammatory responses in the liver. They found that smaller nanoparticles caused more severe immune reactions, including increased neutrophil and macrophage activity and activation of inflammatory signaling pathways. The study provides evidence that nanoplastics can trigger significant immune system disruption in fish even at early life stages.
Nanoplastics in aquatic environments may induce adverse immunotoxicity effects in fish. However, there is insufficient evidence on the visible immunotoxicity endpoints in the larval stages of fish. The liver plays an important role in systemic and local innate immunity in the fish. In this study, the hepatic inflammatory effects of polystyrene (PS) nanoplastic particles (NPs: 100 and 50 nm) and micron PS particles on transgenic zebrafish (Danio rerio) larvae were estimated using fluorescent-labeled neutrophils, macrophages, and liver-type inflammatory binding protein (fabp10a). Particles with smaller size induced higher aggregations of neutrophils and apoptosis of macrophages in the abdomen of the larvae, corresponding to greater hepatic inflammation in the larvae. NPs increased the expression of fabp10a in the larval livers in a dose- and size-dependent manner. PS particles of 50 nm at a concentration of 0.1 mg·L increased the expression of fabp10a in the larval liver by 21.90% (P < 0.05). The plausible mechanisms of these effects depend on their distribution and the generation of reactive oxygen species in the larvae. Metabonomic analysis revealed that the metabolic pathways of catabolic processes, amino acids, and purines were highly promoted by NPs, compared to micron PS particles. NPs also activate steroid hormone biosynthesis in zebrafish larvae, which may lead to the occurrence of immune-related diseases. For the first time, the liver was identified as the target organ for the immunotoxicity effects of NPs in the larval stage of fish.
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This study investigated the hepatotoxic mechanisms of polystyrene nanoplastics in zebrafish (Danio rerio), finding that nanoplastics accumulating in the liver triggered oxidative stress and cellular injury pathways. The results highlight nanoplastics as a significant liver toxicant in aquatic vertebrates.
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Zebrafish larvae exposed to polystyrene micro- and nanoplastics developed kidney damage and weakened immune defenses, making them much more vulnerable to bacterial infection. Both particle sizes suppressed key immune pathways, but nanoplastics primarily caused stress in cells' protein-processing systems while microplastics triggered fat buildup in the kidneys -- showing how different-sized plastic particles can harm health through distinct mechanisms.
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Zebrafish larvae exposed to polystyrene nanoplastics showed significant gut damage, including increased cell death, inflammation, and breakdown of the intestinal barrier. The nanoplastics accumulated in the digestive tract and triggered chemical changes that suggest the plastic particles interact with biological tissue. Since zebrafish share many genetic similarities with humans, these findings raise concerns that nanoplastic ingestion could damage the human gut lining.
Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver
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Researchers exposed zebrafish to polystyrene microplastics of two different sizes and tracked where the particles accumulated in the body. They found that smaller particles (5 micrometers) built up in the gills, liver, and gut, while larger particles (20 micrometers) mainly stayed in the gills and gut. The microplastics caused liver inflammation, oxidative stress, and disrupted fat metabolism, suggesting that ingested microplastics can damage internal organs in fish.
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Polystyrene nanoplastics were shown to be internalized in zebrafish liver cells and accumulate in lysosomes, and while they triggered an immune response in cell cultures, they did not affect larval zebrafish survival in short-term exposures. This suggests that cellular toxicity may not always translate directly to whole-organism mortality at acute exposure levels.
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