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61,005 resultsShowing papers similar to Intracellular Protein Adsorption Behavior and Biological Effects of Polystyrene Nanoplastics in THP-1 Cells
ClearPolystyrene nanoplastics dysregulate lipid metabolism in murine macrophages in vitro
Researchers investigated the effects of polystyrene nanoplastics on immune cell metabolism and found that macrophages exposed to nanoplastics transformed into lipid-laden foam cells. The study suggests that nanoplastic exposure dysregulates lipid metabolism in immune cells, with implications for understanding how these particles may interact with the immune system at the cellular level.
Polystyrene nanoplastics induce profound metabolic shift in human cells as revealed by integrated proteomic and metabolomic analysis
Researchers used integrated proteomic and metabolomic analysis to study how polystyrene nanoplastics affect human kidney and liver cell lines. The study quantified changes in thousands of proteins and hundreds of metabolites, revealing that nanoplastic exposure induced a profound metabolic shift in human cells. Evidence indicates that nanoplastics can be internalized by human cells and trigger significant biological changes at the molecular level.
Toxicological profiling of polystyrene microplastics in raw 264.7 macrophages: Linking microplastic exposure to immune cell impairment
Researchers exposed immune cells called macrophages to polystyrene microplastics and found that the cells rapidly absorbed the particles within two hours. Higher concentrations caused mitochondrial damage, disrupted cellular recycling processes, and triggered inflammation-related signaling. The study provides evidence that microplastics can impair the function of key immune cells responsible for defending the body against foreign threats.
Cell uptake of mixtures of different-sized nanoplastics: Interplay and mechanism
Researchers studied how two sizes of polystyrene nanoplastics interact during cellular uptake, finding that larger 100 nm particles can pull smaller 50 nm particles into cells via clathrin-mediated endocytosis, while smaller particles alter the protein corona of larger ones in serum, either enhancing or inhibiting uptake depending on concentration ratios.
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.
Cellular internalization and release of polystyrene microplastics and nanoplastics
Scientists studied how polystyrene plastic particles of different sizes enter and exit living cells. They found that particles 50 and 500 nanometers in size can penetrate cell membranes and get taken up through multiple pathways, while 5-micrometer particles are too large to enter cells. This research helps explain why smaller nanoplastics may be more harmful to human health, as they can more easily get inside our cells and accumulate there.
Cellular interactions with polystyrene nanoplastics—The role of particle size and protein corona
Researchers investigated how polystyrene nanoplastics interact with mammalian cells, finding that particle size and the protein corona that forms around particles in biological fluids strongly influence cellular uptake and toxicity. Smaller nanoplastics penetrated cell membranes more readily and caused greater disruption, suggesting that the tiniest plastic particles may pose the greatest biological risk.
Exposure to polystyrene nanoplastics impairs lipid metabolism in human and murine macrophages in vitro
Researchers exposed human and mouse macrophages to polystyrene nanoplastics and found that the particles disrupted lipid metabolism in these immune cells. The study observed that nanoplastic exposure altered how macrophages process and store fats, which could affect their ability to function properly. These findings suggest that nanoplastic accumulation in immune cells may interfere with normal metabolic processes at the cellular level.
Polystyrene nanoplastics target lysosomes interfering with lipid metabolism through the PPAR system and affecting macrophage functionalization
Researchers examined how polystyrene nanoplastics affect lysosomal function and lipid metabolism in macrophages through the PPAR signaling system. The study suggests that nanoplastics can interfere with cellular lipid processing by targeting lysosomes, which may affect immune cell function.
Systematic toxicity evaluation of polystyrene nanoplastics on mice and molecular mechanism investigation about their internalization into Caco-2 cells
Researchers fed mice polystyrene nanoplastics (about 100 nm) for 28 days and found the particles accumulated in multiple organs including the spleen, lungs, kidneys, intestines, testes, and brain. The nanoplastics caused cell death, inflammation, and tissue damage in these organs, as well as disrupted fat metabolism and blood cell counts. This study demonstrates that ingested nanoplastics can spread throughout the body and cause widespread harm, raising concerns about long-term human exposure.
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 microplastics induce activation and cell death of neutrophils through strong adherence and engulfment
Researchers found that neutrophils (key immune cells that fight infections) strongly bind to and swallow polystyrene microplastics, mistaking them for bacteria. This triggers inflammation and eventually kills the neutrophils, and the same response was confirmed in both mouse and human immune cells. The findings suggest that microplastics accumulating in the body could weaken immune defenses by destroying these important infection-fighting cells.
Quantification of Polystyrene Uptake by Different Cell Lines Using Fluorescence Microscopy and Label-Free Visualization of Intracellular Polystyrene Particles by Raman Microspectroscopic Imaging
Scientists tested how human cells take up polystyrene microplastic particles using three cell types that represent the lung lining, intestinal lining, and immune system. All three cell types absorbed the microplastic beads, with immune cells showing different uptake patterns compared to the barrier cells of the lungs and gut. This study confirms that microplastics can enter human cells through multiple exposure routes, including breathing and eating, and that immune cells may play a special role in processing these particles.
Cellular response of THP-1 macrophages to polystyrene microplastics exposure
Researchers exposed human macrophage cells to polystyrene nanoparticles smaller than 450 nanometers and observed significant decreases in cell viability, increased oxidative stress, and DNA damage. The particles also reduced mitochondrial membrane potential and inhibited cell proliferation. The findings suggest that microplastic exposure may impair immune cell function in humans, highlighting potential risks to the immune system.
Compromised Autophagic Effect of Polystyrene Nanoplastics Mediated by Protein Corona Was Recovered after Lysosomal Degradation of Corona
Researchers discovered that when polystyrene nanoplastics enter biological environments, proteins coat their surface forming a protective corona that initially reduces their toxic effects on cells. However, once cells internalize the particles and break down the protein layer in lysosomes, the original toxicity returns, including blocked autophagy and lysosomal damage. The study reveals that protein coronas temporarily mask nanoplastic toxicity rather than permanently neutralizing it.
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.
Interfacial Interactions between Nanoplastics and Biological Systems: toward an Atomic and Molecular Understanding of Plastics-Driven Biological Dyshomeostasis
This study investigated how nanoplastics interact with biological molecules at the atomic level, finding that polystyrene nanoplastics can destroy the structure of proteins, disrupt cell membranes, and damage DNA. The nanoplastics essentially unfolded a milk protein, punched holes in cell membranes, and broke DNA strands. These findings help explain at a fundamental level how nanoplastics found in human blood, milk, and tissues could cause the inflammation and disease seen in other studies.
Polystyrene micro(nano)plastics damage the organelles of RBL-2H3 cells and promote MOAP-1 to induce apoptosis
Researchers exposed immune cells to polystyrene particles of different sizes and found that the particles caused oxidative stress, damaged mitochondria and lysosomes, and triggered programmed cell death. The study identified a specific molecular mechanism involving the MOAP-1 protein that drives microplastic-induced cell death, with 50-nanometer particles causing the most severe effects.
Fate of polystyrene micro- and nanoplastics in zebrafish liver cells: Influence of protein corona on transport, oxidative stress, and glycolipid metabolism
Scientists studied how proteins in biological fluids coat nanoplastic particles (forming a "protein corona") and how this coating changes the way cells take up and process the plastics. The protein coating actually increased how many nanoplastics entered liver cells and made them harder to clear out, suggesting that once nanoplastics enter the bloodstream, the body's own proteins may make the contamination harder to eliminate.
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.
The internal dose makes the poison: higher internalization of polystyrene particles induce increased perturbation of macrophages
Researchers exposed human macrophages, key immune cells, to polystyrene particles of different sizes and found that smaller particles were internalized more readily and caused greater cellular disruption. Nanoscale plastics triggered stronger inflammatory responses and more oxidative stress than larger microplastics. The study suggests that the amount of plastic actually absorbed by immune cells, not just the amount present in the environment, determines how harmful the exposure is.
Aging Processes Dramatically Alter the Protein Corona Constitution, Cellular Internalization, and Cytotoxicity of Polystyrene Nanoplastics
Researchers found that aging processes such as UV and ozone exposure dramatically alter how polystyrene nanoplastics interact with blood plasma proteins, form protein coronas, and enter cells. The study suggests that environmentally aged nanoplastics may have different biological effects than pristine particles, which has important implications for accurately assessing the health risks of real-world nanoplastic exposure.
Interaction of polystyrene nanoplastics with human fibrinogen
Researchers found that polystyrene nanoplastics with different surface modifications disrupted the structure of human fibrinogen, a key blood clotting protein, in a dose-dependent manner. The study suggests that nanoplastics entering the bloodstream could interfere with protein function, raising concerns about the potential biological consequences of nanoplastic exposure in humans.
Polystyrene nanoplastics exposure caused defective neural tube morphogenesis through caveolae-mediated endocytosis and faulty apoptosis
This study found that polystyrene nanoplastics caused abnormal neural tube formation in early embryonic development by being taken up through a specific cellular pathway and triggering defective cell death. The findings suggest nanoplastics could potentially interfere with fetal brain development, raising serious concerns about exposure during pregnancy.