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Polystyrene microplastic exposure disrupts mitochondrial pathways and nuclear processes in primary intestinal epithelial cells
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Scientists exposed gut cells to tiny plastic particles (microplastics) and found they threw off normal cell function, ramping up energy production while slowing down processes needed for cell repair and division. This happened more with fresh plastic than plastic that had been through digestion, suggesting how plastics break down in our gut may change how harmful they are. More research is needed to know what this means for long term gut health.
Microplastics are pervasive environmental pollutants that pose a growing concern for human health. Oral ingestion is a common route of human microplastic exposure, yet the proteomic response of the gut epithelium to microplastics remains unclear. This study aimed to investigate the cellular effects of pristine and artificially digested microplastic exposure in primary rat duodenal epithelial cells using untargeted proteomics. Cells were exposed to pristine or digested 0.5 um polystyrene microplastics at 10 or 100 ug/mL for 72 hours and were then analyzed by tandem liquid chromatography and mass spectrometry (LC-MS). Proteins that were both significantly different in intensity compared to controls, with a threshold change of 1.3 or greater, were considered to be differentially expressed. This criterion identified 41 differentially expressed proteins after 100 ug/mL pristine MP exposure, with 19 downregulated and 21 upregulated. Following exposure to 100 ug/mL digested MP, only 3 differentially expressed proteins were upregulated and 7 were down regulated, demonstrating the impact of microplastic physicochemistry. FGSEA pathway analysis revealed that 270 Reactome pathways were significantly altered following microplastic exposure in either condition at both concentrations. These pathways contributed to functional domains including protein synthesis, DNA replication, cell cycle control and aerobic respiration. Overall, microplastic exposure was associated with upregulated mitochondrial respiration, and downregulation of nuclear-related processes including DNA synthesis, transcription and cell proliferation. This study provides targets for future investigation (mitochondria and nucleus) and emphasizes the need to consider biological and environmental conditions for in vitro models of microplastic exposure.
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Polystyrene micro and nano-particles induce metabolic rewiring in normal human colon cells: A risk factor for human health
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Researchers exposed normal human colon cells to polystyrene micro and nanoplastic particles and observed significant metabolic changes in the cells. The study found that these plastic particles altered energy metabolism and cellular pathways in ways that could increase vulnerability to disease. These findings raise concerns that routine ingestion of microplastics through contaminated food may affect normal intestinal cell function in humans.
Cellular and bioenergetic effects of polystyrene microplastic in function of cell type, differentiation status and post-exposure time
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Researchers tested polystyrene microplastics on human lung, colon, and liver cells and found that even a single exposure had lasting effects on cell energy production and caused oxidative stress that continued for 12 days after exposure ended. Colon cells were particularly affected, showing signs of mitochondrial dysfunction long after the initial contact with microplastics. These findings suggest that microplastic exposure through food could cause sustained damage to intestinal cells even after the particles have passed through the body.
The effects of polystyrene microplastics on human intestinal cells health and function
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This study examined how polystyrene microplastics affect normal and cancer intestinal cells, addressing a gap left by previous research that used only cancer cell lines and pristine plastics. The work evaluated microplastic toxicity under more realistic conditions including digestive system biotransformation, assessing effects on nutrient uptake and cellular function.
Probing Long-Term Impacts: Low-Dose Polystyrene Nanoplastics Exacerbate Mitochondrial Health and Evoke Secondary Glycolysis via Repeated and Single Dosing
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This study exposed human intestinal cells to low doses of polystyrene nanoplastics over 12 days and found that repeated exposure caused cumulative damage to mitochondria, the energy-producing structures inside cells. Even concentrations considered environmentally realistic impaired cellular energy production and forced cells to switch to a less efficient backup energy system. This suggests that long-term, everyday nanoplastic exposure through food could gradually harm gut health in ways that might not be immediately noticeable.
Size-dependent effects of polystyrene microplastics on cytotoxicity and efflux pump inhibition in human Caco-2 cells
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Researchers compared how two sizes of polystyrene microplastics affect human intestinal cells grown in the lab. While both sizes showed low direct toxicity, they disrupted mitochondrial function and inhibited important cellular transport pumps that normally help remove harmful substances from cells. The findings suggest that microplastics in the gut could interfere with how intestinal cells handle drugs and toxins, even at concentrations that do not cause obvious cell damage.
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