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61,005 resultsShowing papers similar to Polystyrene nanoplastics target lysosomes interfering with lipid metabolism through the PPAR system and affecting macrophage functionalization
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.
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 and affect lipid metabolism in RTgutGC and head kidney macrophages from Oncorhynchus mykiss
Researchers investigated the subcellular targets of polystyrene nanoplastics in rainbow trout intestinal cells and head kidney macrophages, finding that PS-NPs co-localized with lysosomes but not mitochondria and did not trigger reactive oxygen species production or alter oxidative metabolism. RNASeq analysis further revealed effects on lipid metabolism pathways, indicating that lysosomal targeting and lipid disruption are key mechanisms of nanoplastic toxicity in fish cells.
Effects of micro- and nanoplastic exposure on macrophages: a review of molecular and cellular mechanisms
This review details how macrophages, key immune cells, respond when they engulf micro- and nanoplastics. The particles trigger inflammatory signaling, damage mitochondria and lysosomes, cause excessive production of harmful reactive oxygen species, and can lead to cell death, while in fat tissue they promote fat buildup and insulin resistance.
Lipid metabolic dysregulation: A novel developmental toxicity pathway of aged nanoplastics via inhibition of lipophagy in zebrafish
Researchers showed that UV-aged polystyrene nanoplastics cause more severe developmental toxicity in zebrafish larvae than pristine particles by blocking lipophagy — the cellular process of breaking down stored fat via lysosomes — leading to abnormal lipid accumulation and disrupted early development.
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.
Dietary exposure to polystyrene nanoplastics impairs fasting-induced lipolysis in adipose tissue from high-fat diet fed mice
Researchers demonstrated that fluorescent polystyrene nanoplastics accumulate in the white adipose tissue of mice and can traffic across adipocyte cells. The study found that dietary exposure to nanoplastics impaired fasting-induced fat breakdown in mice fed a high-fat diet, suggesting that nanoplastics may interfere with lipid metabolism and potentially play a role in obesity progression.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
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.
A comparison of the effects of polystyrene and polycaprolactone nanoplastics on macrophages
A comparison of polystyrene and polycaprolactone nanoplastics on macrophage immune cells found both types induced adverse cellular effects, with the study highlighting that plastic persistence in the environment may drive progressive accumulation leading to chronic immune system impacts.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers investigated how macrophages, the immune cells that act as first-line defense in the gut and lungs, respond metabolically to polystyrene microplastic particles. The study found that phagocytosis of microplastics induced an immunometabolic active state in macrophages, suggesting that microplastic exposure may alter immune cell metabolism in ways relevant to understanding potential health effects.
Polystyrene nanoplastics induce lipophagy via the AMPK/ULK1 pathway and block lipophagic flux leading to lipid accumulation in hepatocytes
Polystyrene nanoplastics caused fat to accumulate in human liver cells by disrupting the normal fat-breakdown process called lipophagy. The nanoplastics triggered the cells to start digesting fat droplets but then blocked the final cleanup step by damaging the cell's recycling centers (lysosomes), leaving excess fat trapped inside. This newly identified mechanism helps explain how nanoplastic exposure could contribute to fatty liver disease.
[The effect and mechanism of exposure to polystyrene nanoplastics on lipid metabolism in mice liver].
Researchers exposed mice to 20 nm polystyrene nanoplastics and investigated the effects on hepatic lipid metabolism using multi-omics approaches. Nanoplastic exposure disrupted lipid metabolic pathways in the liver, causing significant changes in lipid accumulation and related gene expression, suggesting a mechanism by which nanoplastic ingestion may contribute to metabolic disorders.
Exposure to polystyrene nanoplastics induces lysosomal enlargement and lipid droplet accumulation in KGN human ovarian granulosa cells
Researchers exposed human ovarian cells to polystyrene nanoplastics and found that the particles entered the cells and caused abnormal enlargement of lysosomes (cellular recycling structures) and accumulation of fat droplets. These changes occurred even at concentrations that did not kill the cells outright, suggesting subtle but potentially significant damage. The findings point to a possible mechanism by which nanoplastics could impair female reproductive health.
Polyvinyl chloride nanoplastics induce lipid metabolism reprogramming of macrophages
This study found that polyvinyl chloride nanoplastics trigger lipid metabolism reprogramming in macrophages, promoting foam cell formation through a lipoprotein-mediated pathway, suggesting a potential mechanism linking nanoplastic exposure to cardiovascular disease risk.
Microplastics released from food containers can suppress lysosomal activity in mouse macrophages
Researchers found that microplastics released from common food containers could suppress immune cell function by impairing lysosomal activity in mouse macrophages. The study tested particles from real commercial packaging materials rather than standard laboratory microplastics, making the findings more relevant to everyday exposure scenarios. These results suggest that microplastic contamination from food packaging may directly affect immune system function.
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.
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 induce glycolipid metabolism disorder via NF-κB and MAPK signaling pathway in mice
Researchers fed mice polystyrene nanoplastics and found that the particles disrupted the animals' ability to regulate blood sugar and fat metabolism. The nanoplastics triggered oxidative stress and inflammation in the liver, activating signaling pathways that led to insulin resistance and abnormal fat accumulation. The study provides evidence that nanoplastic exposure may contribute to metabolic disorders through specific molecular mechanisms involving the NF-kB and MAPK pathways.
Ingestion of micro- and nanoplastic perturbs tissue homeostasis and macrophage core functions
Researchers fed mice polystyrene particles chronically and found that micro- and nanoplastics breached intestinal barriers and accumulated in multiple organs, disrupting tissue homeostasis and impairing core macrophage functions including phagocytosis and inflammatory regulation.
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.
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.
Polystyrene nanoplastics promote adipogenesis by stimulating nuclear translocation of PPARγ
Researchers showed that polystyrene nanoplastics promote fat cell formation in mice and mouse preadipocytes by driving the master fat-cell regulator PPAR-gamma (peroxisome proliferator-activated receptor gamma) into the cell nucleus, where it activates genes that accelerate lipid accumulation and fat tissue expansion.
Cytotoxicity and pro-inflammatory effect of polystyrene nano-plastic and micro-plastic on RAW264.7 cells.
Researchers found that polystyrene nano-plastics (80 nm) induced apoptosis and pro-inflammatory cytokine release in mouse macrophage RAW264.7 cells at lower concentrations than micro-plastics (3 μm), with nano-plastics also enhancing phagocytic activity and activating NF-kB signaling pathways more potently than their larger counterparts.