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61,005 resultsShowing papers similar to Co-Exposure to Polystyrene Microplastics and Bisphenol A Contributes to the Formation of Liver Fibrosis in Mice through Inhibition of the BMAL1/E-Cad Signaling Pathway
ClearLiver Injury Induced by Exposure to Polystyrene Microplastics Alone or in Combination with Cadmium in Mice Is Mediated by Oxidative Stress and Apoptosis
Researchers exposed mice to polystyrene microplastics alone and combined with cadmium over eight weeks to study liver damage. Both exposures caused liver injury through oxidative stress and programmed cell death, but the combination of microplastics and cadmium produced more severe effects. The study suggests that microplastics may worsen the toxic impact of heavy metals on the liver when both are present together.
Combined effect of polystyrene microplastics and bisphenol A on the human embryonic stem cells-derived liver organoids: The hepatotoxicity and lipid accumulation
Researchers used human stem cell-derived liver organoids to study the combined toxic effects of polystyrene microplastics and the plasticizer bisphenol A. The study found that co-exposure produced enhanced hepatotoxicity and lipid accumulation compared to individual exposures, with changes in markers related to oxidative stress, inflammation, and energy metabolism in the liver tissue model.
Implication of ferroptosis in hepatic toxicity upon single or combined exposure to polystyrene microplastics and cadmium
This study found that polystyrene microplastics combined with cadmium caused more severe liver damage in mice than either pollutant alone. The microplastics absorbed cadmium on their surface, increasing the amount of the toxic metal delivered to liver cells, and triggered a type of cell death called ferroptosis. This is concerning because microplastics in the environment commonly carry heavy metals, meaning the combined exposure people face may be more harmful than we thought.
Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway
Researchers found that combined exposure to cadmium and microplastics caused worse liver scarring (fibrosis) in mice than either pollutant alone. The combination triggered a specific inflammatory pathway involving ATP signaling that activated the cells responsible for liver scarring. This is concerning because people are often exposed to both microplastics and heavy metals like cadmium simultaneously through food and water, and the combined effect may be more damaging to the liver than expected.
Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice
Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
Combined exposure of polystyrene microplastics and benzo[a]pyrene in rat: Study of the oxidative stress effects in the liver
Researchers exposed rats to polystyrene microplastics and the carcinogen benzo[a]pyrene, both individually and in combination, to study oxidative stress in liver tissue. The combined exposure caused significantly more liver damage, inflammation, and oxidative stress than either pollutant alone. The study suggests that microplastics may amplify the harmful effects of environmental carcinogens when both are ingested together.
Molecular regulatory networks of microplastics and cadmium mediated hepatotoxicity from NAFLD to tumorigenesis via integrated approaches
This study mapped out how microplastics and the toxic metal cadmium work together to damage the liver, tracing a progression from fatty liver disease to cirrhosis and eventually liver cancer. Cadmium activates genes linked to cell growth and tumor formation, while microplastics trigger cell death pathways related to inflammation. When combined, the two pollutants accelerate liver damage more than either one alone, raising concerns about real-world exposure where people encounter both simultaneously.
Co-exposure to polystyrene microplastics and perfluorooctanoic acid can exacerbate lipid metabolism disorders and liver damage in adult zebrafish
Researchers exposed zebrafish to polystyrene microplastics and the persistent pollutant PFOA separately and together for 28 days, finding that combined exposure caused greater intestinal barrier breakdown, liver damage, lipid metabolism disruption, and gut microbiome dysbiosis than either contaminant alone — raising concerns about nonalcoholic fatty liver disease risk from co-occurring plastic and chemical pollution.
Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
Low-dose polystyrene microplastics exposure increases susceptibility to obesity-induced MASLD via disrupting intestinal barrier integrity and gut microbiota homeostasis
A mouse study found that even low doses of polystyrene microplastics made fatty liver disease significantly worse when combined with a high-fat diet, creating a "double hit" effect. The microplastics damaged the gut lining, disrupted beneficial gut bacteria, and triggered inflammation that spread to the liver, and these harmful effects were difficult to reverse even after two weeks of stopping exposure.
Combined toxicity of polystyrene microplastics and perfluorobutane sulfonate on mouse liver: Impact on lipid metabolism and gut-liver axis disruption
This study examined what happens when mice are exposed to both polystyrene microplastics and PFBS (a type of "forever chemical") at the same time. The combination caused significantly worse liver damage than either pollutant alone, disrupting fat metabolism and triggering gut bacteria imbalances that further harmed the liver through the gut-liver connection. These findings are concerning because microplastics can absorb PFAS chemicals in the environment, meaning people may often be exposed to both together.
Co-exposure to cadmium and microplastics promotes liver fibrosis through the hemichannels -ATP-P2X7 pathway
Researchers investigated co-exposure to cadmium and polystyrene microplastics in a mouse liver fibrosis model, finding that combined exposure promoted liver fibrosis progression through activation of the hemichannel-ATP-P2X7 purinergic signaling pathway, with microplastics acting as a carrier that enhanced cadmium bioavailability and toxicity.
Synergistic Toxicity of Combined Exposure to Acrylamide and Polystyrene Nanoplastics on the Gut–Liver Axis in Mice
Researchers exposed mice to a combination of acrylamide, a common food processing byproduct, and polystyrene nanoplastics through drinking water and found that the combined exposure caused more severe gut and liver damage than either substance alone. The co-exposure disrupted gut barrier integrity, altered gut bacteria composition, and caused widespread metabolic changes. The study suggests that the interaction between nanoplastics and other food contaminants may amplify health risks beyond what each poses individually.
Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver
Mice exposed to microplastics, the plasticizer DEHP, or both together showed liver damage including oxidative stress, cell death, and disrupted metabolism. The combined exposure was worse than either pollutant alone, activating cancer-related genes and impairing the liver's ability to process fats and amino acids. Since DEHP is commonly found alongside microplastics in the environment, these findings suggest that real-world exposure to contaminated plastics could pose a greater liver health risk than previously estimated.
Polystyrene microplastics and di-2-ethylhexyl phthalate co-exposure: Implications for female reproductive health
When rats were exposed to both polystyrene microplastics and the common plasticizer DEHP together, they developed significantly more ovarian damage -- including increased cystic follicles, fibrosis, and hormone imbalance -- than from either substance alone. The combined exposure activated a specific signaling pathway (TGF-beta1/Smad3) linked to ovarian fibrosis and may increase the risk of polycystic ovary syndrome, raising concerns about real-world co-exposure in women.
Distinct toxicity of microplastics/TBBPA co-exposure to bioprinted liver organoids derived from hiPSCs of healthy and patient donors
Using 3D-bioprinted liver tissue models grown from human stem cells, researchers found that microplastics combined with the flame retardant TBBPA caused greater liver damage than either substance alone. The study suggests that microplastics may worsen the toxic effects of environmental chemicals on liver tissue, and that people with pre-existing liver conditions could be more vulnerable.
Combined Enterohepatic Toxicity of Polystyrene Microplastics and Di(2-ethylhexyl) Phthalate in Mice: Gut Microbiota-Dependent Synergistic Effects
Researchers investigated the combined toxicity of polystyrene microplastics and the plasticizer DEHP in mice, focusing on gut-liver axis effects. They found that co-exposure worsened harmful outcomes compared to either pollutant alone, with gut microbiota playing a key mediating role in the synergistic toxicity. The study suggests that microplastics and their associated chemical additives may interact to amplify health risks through disruption of the gut-liver connection.
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.
Toxicity of polyethylene terephthalate microplastics and dimethyl phthalate in male Sprague-Dawley rats: Insights into oxidative stress, DNA damage, and histopathological impacts
Researchers exposed male rats to polyethylene terephthalate microplastics and dimethyl phthalate, a common plasticizer, both individually and in combination over 28 days. The co-exposure group showed significantly elevated markers of oxidative DNA damage, severe liver tissue degeneration, and liver enlargement compared to controls. The study highlights the potential for synergistic health effects when microplastics and their associated chemical additives are encountered together.
Combined exposure of nano‐titanium dioxide and polystyrene nanoplastics exacerbate oxidative stress‐induced liver injury in mice by regulating the Keap‐1 / Nrf2 / ARE pathway
Researchers found that mice exposed to both polystyrene nanoplastics and nano-titanium dioxide together suffered worse liver damage than those exposed to either substance alone. The combined exposure amplified oxidative stress and disrupted a key protective signaling pathway in the liver, suggesting that co-exposure to multiple nanoparticles may pose greater health risks than individual exposures.
Oral exposure to polyethylene microplastics induces inflammatory and metabolic changes and promotes fibrosis in mouse liver.
Mice fed polyethylene microplastics in their food for 6 to 9 weeks developed liver inflammation, metabolic disruption, oxidative stress, and increased cell growth in the liver. The microplastics also worsened liver scarring (fibrosis) when tested in mice with pre-existing liver damage. This is the first study to show that ingesting polyethylene, the most common type of plastic, can directly damage the mammalian liver and could worsen existing liver conditions.
Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38 MAPK/p65 NF‐κB Signaling Pathway
Researchers found that exposure to PET microplastics induced liver fibrosis in mice through oxidative stress and activation of the p38 MAPK/p65 NF-kB signaling pathway. The study suggests that PET microplastics, which are frequently detected in both environmental samples and human tissues, may contribute to liver damage through inflammatory and oxidative mechanisms.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.