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Polystyrene microplastics with different sizes induce the apoptosis and necroptosis in liver through the PTEN/PI3K/AKT/autophagy axis
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Mice exposed to polystyrene microplastics of different sizes developed liver damage through two types of cell death: apoptosis and necroptosis. Smaller microplastics caused more severe damage, disrupting a key cell survival pathway called PTEN/PI3K/AKT and impairing the liver's self-cleaning process (autophagy). The study suggests that the smallest microplastic particles may pose the greatest liver health risk because they penetrate cells more readily.
The production of plastics worldwide has been instrumental in the progress of modern society, while the increasing accumulation of plastics castoff in oceans, soils and anywhere else has become a major pressure source on environmental sustainability and animal health. Meanwhile, from a biological perspective, our understanding of the toxicological fingerprints of plastics, especially microplastics (MPs), is still poor. Here, we reported a phenomenon of hepatotoxicity dominated by MPs in the form of polystyrene (PS), was observed in mice model systems and cellular assays. Apoptosis and necroptosis related to the size of particles were seen upon PS-MPs introduction, as revealed by transmission electron microscopy, fluorescence microscopy, flow cytometry, and quantitative analysis of signaling pathways in vivo and vitro. Collectively, the current study demonstrated that the levels of liver cell injury caused by PS-MPs were negatively correlated with the particle diameters. Small-sized particles (1-10 μm) induced cell death primarily as necroptosis whereas the large-sized particles (50-100 μm) mainly induced apoptosis, which was directly accomplished by PTEN/PI3K/AKT signaling axis and its targeted autophagy flux. More interestingly, inhibition of autophagy not only alleviated PS-MPs-triggered cell death, but also changed the form of death injury to a certain extent. This uncovered crosstalk relationship opens up a new avenue for investigating the biological and toxicological effects of MPs, and may provide important insights for preventing and limiting of health hazards from MPs.
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
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Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size
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Researchers exposed mouse liver cells to polystyrene microplastics of different sizes and found that smaller particles caused more oxidative stress and damage than larger ones. The microplastics disrupted protective antioxidant systems and increased harmful reactive oxygen species inside the cells. This suggests that the smallest microplastic particles may pose the greatest risk to liver health because they can enter cells more easily and cause more internal damage.
Proteomics reveals that nanoplastics with different sizes induce hepatocyte apoptosis in mice through distinct mechanisms involving mitophagy dysregulation and cell cycle arrest
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Mice fed diets containing 100 nm polystyrene nanoplastics for 180 days showed more hepatocyte apoptosis than those fed 500 nm particles, with proteomic analysis revealing size-dependent mechanisms involving Pdcd2l-mediated cell cycle arrest and distinct mitophagy dysregulation pathways.
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