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Detection of Time-Dependent Uptake of Microplastics by Joint Utilization of Hepatic Organoids and a 3D-Printed Carrier
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Scientists grew tiny lab-made liver tissues (organoids) that behave more like real livers than flat cell cultures, and found they absorbed surprising amounts of microplastic particles, nearly 40% within 48 hours. This uptake damaged liver cells and impaired their energy-producing mitochondria, suggesting microplastics may pose a real risk to liver health, not just a theoretical one.
Microplastics (MPs, <5 mm) are pervasive in foods, the environment, and humans, posing emerging health risks. Traditional two-dimensional (2D) cell models inadequately replicate micron-scale MP uptake, whereas three-dimensional (3D) organoids better mimic tissue complexity. Here, we developed a hepatic organoids (HOs)-in-cage system using human pluripotent stem cell-derived HOs and a 3D-printed porous poly(ε-caprolactone) carrier for efficient organoid retrieval. We established a label-free Nile Red (NR)-based spatiotemporal imaging and flow cytometric quantification pipeline to investigate the uptake dynamics and hepatotoxicity of UV-aged, size-mixed polypropylene (PP, 1 to 20 μm), as well as to colocalize the MP and potential biomarkers within HOs. Contrary to 2D models where >5 μm particles show negligible internalization, 3D HOs exhibited significant accumulation of intact micron-scale MPs via tissue-layer penetration and paracellular retention, with PP uptake peaking at ∼40% within 48 h and ∼18% retained long-term. This triggered dose- and time-dependent hepatotoxicity (40-4000 ng/mL), marked by CD36 upregulation from 8 h, mitochondrial impairment, and elevated LDH and AST levels. Notably, NR fluorescence intensity was governed by polymer chemistry rather than surface roughness, enabling material-specific detection. This work provides novel label-free techniques within 3D in vitro models to explore the depot and effective concentration of micron-scale MPs, advancing understanding of MP-induced cellular damage upon uptake and deposition.
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Using human liver organoids (miniature lab-grown livers), researchers found that sun-aged microplastics caused more damage to liver cells than fresh microplastics, even at concentrations matching what is found inside human bodies. The aged particles specifically disrupted energy production in mitochondria and altered an amino acid metabolism pathway linked to cardiovascular disease. This is significant because most microplastics in the environment have been weathered by sunlight, meaning the real health risk may be greater than studies using pristine plastics suggest.
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Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
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Using an advanced gut-liver organ-on-a-chip system that mimics human digestion, researchers tracked how polystyrene microplastics travel from the intestine to the liver. The microplastics crossed the intestinal barrier, accumulated in liver tissue, and caused dose-dependent damage to liver cells. This human-relevant model provides strong evidence that microplastics ingested through food and water can reach and harm the liver.
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Scientists grew tiny lab-made liver models and exposed them to common plastic particles (from water bottles, packaging, and other everyday plastics) for three weeks to see what happens when liver cells are around microplastics long-term. The plastics didn't kill the liver cells outright, but they did change how the cells produce and use energy, a subtler effect that could add up over time. This matters because it gives researchers a better tool to study how different types of plastic might quietly affect liver health, even without causing obvious damage.
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Researchers developed a digestive system organ-on-a-chip microphysiological platform to assess how nanoplastics (NPs) are absorbed, metabolized, and cause internal exposure risks. The system revealed size-dependent toxic effects of NPs on liver cells and lipid metabolism, providing mechanistic insights into NP-associated liver disease risk.
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