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61,005 resultsShowing papers similar to Increased clearance of non-biodegradable polystyrene nanoplastics by exocytosis through inhibition of retrograde intracellular transport
ClearAlleviation of neurotoxicity induced by polystyrene nanoplastics by increased exocytosis from neurons
Researchers investigated how polystyrene nanoplastics accumulate in neurons and cause toxic effects on brain cells. They found that inhibiting a specific protein involved in transporting particles within cells promoted the export of nanoplastics from neurons, reducing their harmful effects. The study suggests that enhancing the cell's natural ability to expel nanoplastics could be a potential strategy for alleviating their neurotoxic impact.
Interactions between polystyrene nanoparticles and human intestinal epithelial Caco-2 cells
Researchers traced how 70 nm polystyrene nanoplastics enter and exit human intestinal Caco-2 cells, finding that particles accumulate in lysosomes and mitochondria over 72 hours and are cleared primarily through the lysosomal pathway, with serum in the medium inhibiting that clearance.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
Researchers demonstrated that polystyrene nanoplastics can cross the blood-brain barrier and accumulate in mouse brains, leading to cognitive impairment and loss of connections between brain cells. The damage was driven by excessive splitting of mitochondria, the energy-producing structures within cells, which triggered runaway cellular cleanup processes. Importantly, a drug that blocks this mitochondrial splitting reversed the cognitive damage, suggesting a potential therapeutic approach to nanoplastic-related brain injury.
Stress Response of Mouse Embryonic Fibroblasts Exposed to Polystyrene Nanoplastics
Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
Crossing barriers – tracking micro- and nanoplastic pathways into the human brain
Researchers tracked potential pathways by which micro- and nanoplastics may enter the human brain, examining both in vitro cell models and post-mortem brain tissue. They found that human monocytes rapidly internalized polystyrene particles into endocytic vesicles and mitochondria, and detected plastic particles in brain tissue samples, providing evidence that nanoplastics may be capable of crossing brain barriers.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
Polystyrene nanoplastics affect the human ubiquitin structure and ubiquitination in cells: a high-resolution study
Using NMR and TEM analyses, polystyrene nanoplastics were shown to form a hard protein corona with human ubiquitin and to impair ubiquitination in HeLa cells, revealing a potential mechanism by which nanoplastic exposure disrupts protein degradation pathways in human cells.
Polystyrene Nanoplastics Increase Macrophage Bactericidal Activity Through a Mechanism Involving Reactive Oxygen Species and Itaconate
Researchers found that polystyrene nanoplastics internalised by macrophages accumulated in endosomes, lysosomes, and the endoplasmic reticulum, enhancing bacterial killing through a mechanism involving increased reactive oxygen species production and itaconate signalling. The results suggest that nanoplastic exposure may paradoxically boost certain innate immune functions.
Microglial clearance of Alzheimer's amyloid-beta obstructed by nanoplastics
Researchers found that polystyrene nanoplastics interfere with the brain's ability to clear amyloid-beta, the protein that builds up in Alzheimer's disease. The nanoplastics accelerated amyloid clumping and drained the energy of brain immune cells that normally clean up these harmful proteins. This study suggests that nanoplastic exposure could worsen or contribute to the development of Alzheimer's disease.
Primary astrocytes as a cellular depot of polystyrene nanoparticles
Researchers found that astrocytes — support cells in the brain — absorb polystyrene nanoplastics far more efficiently than neurons and act as a cellular buffer to protect nerve cells, but become overactivated when the particle load is too high, losing their protective function and potentially contributing to neurological harm.
Lysosomal dependent transcytosis of polystyrene nanoplastics within macrophages
Researchers studied how nanoplastics are transported through human macrophages via lysosomal-dependent transcytosis, tracking the complete intracellular migration pathway including internalization, vesicular trafficking, and exocytosis. The findings reveal that macrophages can transport nanoplastics across cellular barriers, potentially facilitating their distribution to distant tissues.
Nanoplastics in the Environment: Sources, Fate, Toxicity, Challenges and Mitigation Strategies
This review covers the formation, environmental fate, and health risks of nanoplastics, emphasizing their capacity to penetrate biological barriers and cause oxidative stress, inflammation, DNA damage, and endocrine disruption, alongside current strategies for mitigation.
Polystyrene Nanoplastics Induce Neutrophil Extracellular Traps in Mice Neutrophils
Researchers discovered that polystyrene nanoplastics trigger the release of neutrophil extracellular traps in mouse immune cells through reactive oxygen species and PAD4-mediated chromatin depolymerization, revealing a previously unknown immunotoxicity mechanism.
A new mechanism for ubiquitination in polystyrene nanoplastic-induced spatial cognitive dysfunction through microglial activation-induced apoptosis of neurons
Researchers found that polystyrene nanoparticles disrupt microglial lipid metabolism in the brain by suppressing the protein RNF139, which leads to SREBP activation, mitochondrial dysfunction, and inflammatory signaling that ultimately kills neurons and impairs spatial memory in mice.
Polystyrene Micro- and Nanoplastic Exposure Triggers an Activation and Stress Response in Human Astrocytes
Researchers exposed primary human astrocytes to polystyrene micro- and nanoplastics and found that these particles triggered cellular stress responses, including increased production of reactive oxygen species and activation of inflammatory pathways. Nanoplastics were particularly effective at penetrating cells and disrupting normal astrocyte function. The findings suggest that plastic particle exposure may contribute to neuroinflammatory processes in the brain, warranting further investigation into potential neurotoxic effects.
Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
Cytotoxic and dysmetabolic impact of polystyrene nanoplastics, a new potential atherosclerotic cardiovascular risk factor, on a steatosis model of HepG2 cells
Researchers exposed cell cultures to polystyrene nanoplastics and found significant cytotoxic effects and metabolic disruption including mitochondrial dysfunction and altered glucose metabolism, suggesting nanoplastics may act as a novel class of metabolic disruptors.
Nanoplastics and Immunity: Investigating the Extracellular Matrix’s Influence on Macrophage Interaction with Polystyrene Nanoparticles
Researchers investigated how extracellular matrix components affect macrophage uptake of polystyrene nanoplastics, finding that the surrounding matrix modulates nanoplastic-immune cell interactions — with implications for understanding how nanoplastics evade or engage the innate immune response.
Recognition and movement of polystyrene nanoplastics in fish cells
Researchers tracked how zebrafish cells take up, transport, and release three types of polystyrene nanoplastics with different surface modifications. They found that cell uptake peaked within two hours and occurred mainly through specific cellular pathways, with the particles initially entering the cytoplasm before being transported to lysosomes. The nanoplastics were retained in cells for 10 to 15 hours depending on surface chemistry, highlighting the importance of understanding how these particles move through biological systems.
Investigation of Cell-to-cell Transfer of Polystyrene Microplastics Through Extracellular Vesicle-mediated Communication
Researchers investigated cell-to-cell transfer of polystyrene microplastics through extracellular vesicles, finding that cells can package and transfer plastic particles via vesicle-mediated pathways, a previously unrecognized route for intracellular plastic dissemination.
Polystyrene nanoplastics trigger pyroptosis in dopaminergic neurons through TSC2/TFEB-mediated disruption of autophagosome-lysosome fusion in Parkinson’s disease
This study found that polystyrene nanoplastics accelerated the onset and progression of Parkinson's disease in lab models by disrupting the brain cells' waste-clearing system. The nanoplastics interfered with how brain cells break down damaged proteins, triggering a type of inflammatory cell death in the dopamine-producing neurons that are critical for movement control.
Blood uptake and urine excretion of nano- and micro-plastics after a single exposure.
Mice exposed to polystyrene nanoparticles (100 nm) and microparticles (3 µm) via different routes showed that smaller particles appeared rapidly in blood and were detected in urine, while larger particles cleared more slowly. The study provides direct evidence that nanoplastics can cross biological barriers and enter circulation, with potential for distribution throughout the body.
Unmasking the Invisible Threat: Biological Impacts and Mechanisms of Polystyrene Nanoplastics on Cells
This review summarizes how polystyrene nanoplastics, tiny plastic particles found throughout the environment, damage cells through multiple pathways including oxidative stress, DNA damage, inflammation, and mitochondrial dysfunction. Nanoplastics can trigger several forms of cell death and disrupt normal cell processes like autophagy (the cell's recycling system). The findings raise concerns about long-term human health effects from chronic exposure to these nearly invisible plastic particles.
Polystyrene Nanoplastics Activate Autophagy and Suppress Trophoblast Cell Migration/Invasion and Migrasome Formation to Induce Miscarriage
In mouse and cell studies, polystyrene nanoplastics at doses near real-world human exposure levels caused miscarriage by blocking the movement of placental cells needed for a healthy pregnancy. The nanoplastics triggered a cellular recycling process called autophagy that broke down key proteins required for placental cell migration and invasion.