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61,005 resultsShowing papers similar to The size-dependence and reversibility of polystyrene nanoplastics-induced hepatic pyroptosis in mice through TXNIP/NLRP3/GSDMD pathway
ClearThe size-dependence and reversibility of polystyrene nanoplastics-induced lipid accumulation in mice: Possible roles of lysosomes
This mouse study found that smaller nanoplastics (100 nm) cause more fat buildup in the liver than larger ones (500 nm), showing that size matters when it comes to health effects. Encouragingly, the liver damage was reversible after the mice stopped being exposed, suggesting the body can recover once nanoplastic intake is reduced. The damage appears to work by disrupting the cell's waste-recycling system (lysosomes).
Biological interactions of polystyrene nanoplastics: Their cytotoxic and immunotoxic effects on the hepatic and enteric systems
Researchers exposed mouse and human liver cells and live mice to polystyrene nanoplastics of five different sizes and found that the smallest particles were most toxic in lab dishes, while medium and large particles caused the most liver damage in living animals. The larger particles triggered immune responses by recruiting inflammatory cells to the liver and intestines, causing tissue damage. This study reveals that nanoplastic size matters in unexpected ways, and that lab tests alone may not predict which particles are most dangerous in the body.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
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 exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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 nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
Polystyrene Nanoplastics Induce Pyroptosis in HepG2 Cells via the YAP1-cGAS-STING Signaling Axis.
Scientists found that tiny plastic particles from polystyrene (commonly used in disposable cups and food containers) can trigger a harmful type of cell death in liver cells. When these microscopic plastic pieces enter liver cells, they activate a specific pathway that causes the cells to essentially self-destruct, which could potentially damage the liver over time. This research helps explain how the plastic pollution we're exposed to daily might be harming our bodies, particularly our liver health.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice
Mice and liver cells exposed to 20-nanometer polystyrene nanoplastics developed liver damage through a specific molecular pathway involving oxidative stress and inflammation. The study showed that activating the body's natural antioxidant defense system (called NRF2) could protect against this liver injury, offering a potential avenue for reducing nanoplastic-related harm to human liver health.
Polystyrene microplastics with different sizes induce the apoptosis and necroptosis in liver through the PTEN/PI3K/AKT/autophagy axis
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.
Distinctive lipidomic responses induced by polystyrene micro- and nano-plastics in zebrafish liver cells
Researchers compared how micro-sized and nano-sized polystyrene plastic particles affect fat metabolism in zebrafish liver cells. They found that both sizes were taken up by cells, but the smaller nanoplastics caused more pronounced disruptions to lipid profiles and triggered cell death pathways. The findings underscore that particle size matters when assessing the biological impact of plastic pollution on fish.
Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.
Effects of polystyrene micro/nanoplastics on liver cells based on particle size, surface functionalization, concentration and exposure period
Researchers systematically studied the effects of polystyrene micro- and nanoplastics on human liver cells, varying particle size, surface chemistry, concentration, and exposure duration. They found that smaller particles were internalized more readily and that surface functionalization significantly influenced toxicity, with aminated particles causing the most cell damage. The study suggests that particle characteristics beyond just size play an important role in determining how micro- and nanoplastics affect human cells.
Proteomics reveals that nanoplastics with different sizes induce hepatocyte apoptosis in mice through distinct mechanisms involving mitophagy dysregulation and cell cycle arrest
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.
[Exposure Pathways of Polystyrene Nanoplastics Mediate Their Cellular Distribution and Toxicity].
This study found that the route by which polystyrene nanoplastics enter the body determines which liver cell types accumulate the particles and what toxic effects occur, demonstrating that exposure pathway—not just dose—shapes nanoplastic toxicity in hepatic tissue.
Integrative lipidomic and transcriptomic analysis unraveled polystyrene nanoplastics-induced liver injury via oral and inhalation exposure: All roads lead to Rome?
Researchers exposed mice to polystyrene nanoplastics through both oral ingestion and inhalation, and found that both routes caused liver damage but through different molecular pathways. Oral exposure mainly caused visible tissue damage, while inhaled nanoplastics triggered more severe inflammation and impaired the liver's ability to produce essential proteins. The study reveals that breathing in nanoplastics may be just as harmful to the liver as swallowing them, with different but equally concerning effects.
Polystyrene Microplastics Induce Oxidative Stress in Mouse Hepatocytes in Relation to Their Size
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.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
The role of gut microbiota in mediating increased toxicity of nano-sized polystyrene compared to micro-sized polystyrene in mice
This mouse study found that nano-sized polystyrene plastics were significantly more toxic than micro-sized ones, causing greater gut inflammation, liver damage, and metabolic disruption. The key difference was driven by how each size affected gut bacteria: nanoplastics caused a more severe shift toward harmful bacteria and away from beneficial ones. The findings suggest that the smallest plastic particles may pose the greatest health risk because they more dramatically disrupt the gut microbiome.
Polystyrene microplastics cross the murine intestine and induce inflammatory cell death after phagocytosis by human monocytes and neutrophils
Researchers orally administered 1 μm and 10 μm polystyrene particles to mice for 10 days and found that both sizes crossed the intestinal epithelium and were detected in blood and liver; when phagocytosed by human monocytes and neutrophils, the particles triggered complement-dependent inflammatory cell death.
Intranasal exposure to UV-irradiated polystyrene nanoplastics triggers vital organ inflammation and cognitive impairment
Researchers exposed rats to polystyrene nanoplastics through nasal passages and found that UV-irradiated particles caused more severe damage than pristine ones, triggering inflammation in the lungs, liver, and kidneys. Smaller 100-nanometer particles caused more serious liver damage than larger 600-nanometer particles, as indicated by elevated liver enzyme levels. The study also found that learning and memory abilities declined as the duration of nanoplastic photoaging increased.
Immunotoxicity responses to polystyrene nanoplastics and their related mechanisms in the liver of zebrafish (Danio rerio) larvae
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.
Co-exposure to polystyrene nanoplastics and glyphosate exacerbates NETs-mediated pyroptosis by activating the NLRP3 inflammasome in mouse liver
Researchers found that co-exposing mice to polystyrene nanoplastics and the herbicide glyphosate caused significantly worse liver damage than either pollutant alone. The combined exposure triggered a chain of inflammatory events including immune cell infiltration, formation of neutrophil traps, and cell death in liver tissue, all driven by activation of a key inflammatory pathway called NLRP3. The study suggests that nanoplastics may amplify the harmful effects of common agricultural chemicals when they enter the body together.
Size- and oxidative potential-dependent toxicity of environmentally relevant expanded polystyrene styrofoam microplastics to macrophages
Researchers tested how Styrofoam microplastics of different sizes and weathering conditions affect human immune cells and found that smaller particles, UV-weathered particles, and those from real-world sources were all more toxic. The microplastics triggered inflammation through a pathway called the NLRP3 inflammasome, which is linked to many chronic diseases. This is concerning because most Styrofoam in the environment has been weathered by sunlight, meaning the real-world health risks may be worse than lab studies using fresh materials suggest.