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Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp
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Researchers exposed carp to polyethylene microplastics and found they caused serious intestinal damage through two harmful pathways: ferroptosis (a type of iron-dependent cell death) and NF-kB-driven inflammation. The microplastics triggered a buildup of iron and reactive oxygen species in gut tissue, leading to cell death and tissue destruction. Since humans also ingest microplastics that reach the gut, these findings highlight a potential mechanism by which microplastics could damage our digestive system.
Microplastics (MPs), a new class of pollutant that threatens aquatic biodiversity, are becoming increasingly prevalent around the world. Fish growth may be severely inhibited by microplastics, resulting in severe mortality. Exposure to microplastics increases the likelihood of intestinal injuries, but the underlying mechanisms remain equivocal. The objective of this study was to investigate the potential toxic mechanisms underlying microplastic-induced intestinal injury in fish and to assist researchers in identifying novel therapeutic targets. In this study, a model of carp exposed to microplastics was established successfully. Histological observation showed that exposure to polyethylene microplastics caused damage to the intestinal mucosal surface and a significant increase in goblet cells, which aggregated on the surface of the mucosa. The mucosal layer was observed to fall off. Lymphocytes in the intestinal wall proliferated and aggregated. TUNEL staining showed that apoptosis occurred in the group exposed to microplastics. The qPCR results showed that the expression of Ferroptosis apoptotic factors COX-2 and ACSL4 was upregulated, while the expression of TFRC, FIH1, SLC7A11, and GPX4 was downregulated. The NF-κB pathway (p-p65, IκBα), inflammatory cytokines (TNF-α, IL-8, IL-6) and apoptosis genes (Bax, Caspase3) were upregulated. Semi-quantitative detection of related proteins by Western blotting was consistent with the gene expression results. In addition, the ELISA assay showed that lipid peroxidation and inflammatory cytokines (TNF-α, IL-1β, IL-6) were increased in the microplastic exposed group. To conclude, lipid peroxidation induced by microplastics activates the NF-κB pathway and causes ferroptosis, ultimately resulting in intestinal damage and cellular apoptosis.
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Ferroptosis Induced by Micro/Nanoplastics: Mechanisms, Toxic Effects, and Implications for Aquaculture
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This review summarizes existing research on how tiny plastic particles (microplastics and nanoplastics) can trigger a type of cell death called ferroptosis in farmed aquatic animals, damaging organs like the intestine, liver, and gills. It describes the biological mechanisms involved and discusses possible monitoring markers and management approaches for aquaculture settings.
Polystyrene microplastics induce endoplasmic reticulum stress, apoptosis and inflammation by disrupting the gut microbiota in carp intestines
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Researchers fed carp polystyrene microplastics and found that the particles disrupted their gut bacteria, killing off beneficial species and promoting those linked to diseases. The microplastics triggered a stress response in intestinal cells that led to inflammation, cell death, and tissue damage. Since carp is a widely eaten fish, these gut health effects raise questions about how microplastics in aquatic environments could affect the safety of fish that humans consume.
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This study found that polystyrene microplastics harmed juvenile fish by triggering immune dysfunction, oxidative stress, and mitochondrial damage in their intestines. The microplastics activated inflammatory pathways, damaged the intestinal barrier, and shifted the gut microbiome toward harmful bacteria. These findings suggest that microplastic ingestion could have cascading effects on fish health through multiple biological pathways.
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Molecular mechanism differences between nanoplastics and microplastics in colon toxicity: nanoplastics induce ferroptosis-mediated immunogenic cell death, while microplastics cause cell metabolic reprogramming
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This study discovered that nanoplastics and microplastics damage the colon through completely different mechanisms depending on their size: nanoscale particles (100 nm) get inside cells and trigger a type of cell death called ferroptosis, while larger particles (10 micrometers) cause physical damage and force cells to switch their energy production. These findings suggest that the smallest plastic particles may pose unique health risks to the gut that differ from larger ones.
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