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61,005 resultsShowing papers similar to Distinct toxicity of microplastics/TBBPA co-exposure to bioprinted liver organoids derived from hiPSCs of healthy and patient donors
ClearCombined 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.
Toxicity of microplastics and plastic additive co-exposure in liver Disse organoids from healthy donors and patient-derived induced pluripotent stem cells
Researchers biofabricated liver Disse-like organoids from both healthy donor cells and patient-derived induced pluripotent stem cells (hiPSCs) to investigate the combined toxicity of microplastics and plastic additives, which typically co-exist in the environment as complexes that enter human blood circulation. The organoid model revealed that microplastic and additive co-exposure increased risks of steatohepatitis-related pathological responses in hepatic tissue.
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.
The combined toxicity of polystyrene nano/micro-plastics and triphenyl phosphate (TPHP) on HepG2 cells
This study found that polystyrene nanoplastics and microplastics made a common flame retardant chemical (TPHP) more toxic to human liver cells than the chemical alone. The nanoplastics absorbed the flame retardant and delivered it to cells, causing increased oxidative stress, mitochondrial damage, and cell death. Smaller nanoplastics caused more harm than larger microplastics, suggesting that as plastics break down into smaller pieces, their ability to carry toxic chemicals into human cells increases.
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.
Prenatal High-Fat Diet Combined with Microplastic Exposure Induces Liver Injury via Oxidative Stress in Male Pups
Researchers studied the combined effects of a maternal high-fat diet and microplastic exposure on liver health in newborn rat pups. They found that the combination caused more severe liver fat accumulation and oxidative stress damage than either factor alone. The study suggests that prenatal exposure to both microplastics and an unhealthy diet may compound the risk of liver injury in offspring.
Influence of polystyrene nanoparticles on the toxicity of tetrabromobisphenol A in human intestinal cell lines
When human intestinal cells were exposed to both polystyrene nanoparticles and the flame retardant TBBPA together, the chemical pollutant dominated the toxic response, causing oxidative stress, DNA damage, and disruption of mitochondrial function. The study shows that mixing microplastics with other contaminants can produce complex, hard-to-predict health effects in gut cells, which matters because people are routinely exposed to multiple pollutants at once.
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.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
Liver 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.
Influence of the co-exposure of microplastics and tetrabromobisphenol A on human gut: Simulation in vitro with human cell Caco-2 and gut microbiota
Researchers studied the combined effects of polyethylene microplastics and the flame retardant TBBPA on human gut cells and gut bacteria in laboratory experiments. The study found that both substances damaged human intestinal cells, with TBBPA playing the larger role, while microplastics amplified certain harmful effects at high concentrations. TBBPA also selectively killed beneficial gut bacteria like Lactobacillus while promoting potentially harmful species, and microplastics enhanced this imbalance.
Microplastic-contaminated antibiotics as an emerging threat to mammalian liver: enhanced oxidative and inflammatory damages
Researchers used a mouse model to study what happens when microplastics contaminated with antibiotics are ingested together, simulating real-world food chain exposure. The study found that the combination caused enhanced oxidative stress and inflammatory damage in the liver compared to either pollutant alone. The findings suggest that microplastics carrying adsorbed antibiotics may pose a greater threat to liver health than microplastics or antibiotics individually.
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.
Effects of microplastics (MPs) and tributyltin (TBT) alone and in combination on bile acids and gut microbiota crosstalk in mice
Researchers studied the combined effects of microplastics and tributyltin (TBT), an environmental pollutant, on bile acid metabolism and gut microbiota in mice. The study found that both individual and combined exposures induced liver inflammation, altered gut microbial composition, and disturbed bile acid profiles, suggesting that co-exposure to microplastics and chemical pollutants may have compounding effects on gut health.
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.
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
Researchers found that co-exposure to polystyrene microplastics and bisphenol A caused liver fibrosis in mice by disrupting a key signaling pathway that controls cell adhesion. The combined exposure produced more severe liver damage than either substance alone, with excessive buildup of scar tissue in the liver. The study suggests that the widespread co-occurrence of microplastics and BPA in food packaging could pose synergistic risks to liver health.
Integrated transcriptomics and metabolomics to explore the varied hepatic toxicity induced by aged- and pristine-microplastics: in vivo and human-originated liver organoids-based in vitro study
Using human liver organoids (miniature lab-grown livers), researchers found that sun-aged microplastics caused more damage to liver cells than fresh microplastics, even at concentrations matching what is found inside human bodies. The aged particles specifically disrupted energy production in mitochondria and altered an amino acid metabolism pathway linked to cardiovascular disease. This is significant because most microplastics in the environment have been weathered by sunlight, meaning the real health risk may be greater than studies using pristine plastics suggest.
Synergistic toxicity of PFAS and microplastic mixtures across five human cell lines
Researchers tested the combined toxicity of PFAS chemicals and microplastics on five types of human cells representing the kidney, liver, prostate, skin, and lung. They found that mixtures of these common environmental contaminants produced synergistic harmful effects, particularly in kidney and liver cells, including increased oxidative stress and DNA damage. The study suggests that the combined exposure to PFAS and microplastics, which frequently co-occur in the environment, may pose greater health risks than either pollutant alone.
Microplastic-induced hepatic adverse effects evaluated in advanced quadruple cell human primary models following three weeks of repeated exposure
Scientists tested the effects of microplastics on a sophisticated model of human liver cells over three weeks of repeated exposure, finding that certain microplastic types triggered inflammation and altered liver function. The advanced cell model, which combines four types of human liver cells, provides more realistic results than simpler lab tests. These findings add to growing evidence that microplastics accumulating in the liver could contribute to chronic inflammation and liver damage in humans.
Gut–Liver Axis Mediates the Combined Hepatointestinal Toxicity of Triclosan and Polystyrene Microplastics in Mice: Implications for Human Co-Exposure Risks
Mice co-exposed to the antimicrobial triclosan and polystyrene microplastics showed markedly worse intestinal and liver damage than those exposed to either contaminant alone, with gut microbiome disruption identified as a key mediating mechanism.
Microplastics and plastic additives as contaminants of emerging concern: A multi-biomarker approach using Rhinella arenarum tadpoles
Researchers exposed toad tadpoles to polyethylene microplastics and the flame retardant TBBPA, both alone and in combination, for 30 days. They found that the mixture produced different toxic effects than either substance alone, affecting growth, enzyme activity, and cellular stress markers. The study highlights the importance of studying microplastics alongside common plastic additives, since their combined effects may differ from individual exposures.
Lipidomic analysis of single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human hepatoma cells
Researchers used lipidomic analysis to study the single and combined effects of polyethylene microplastics and polychlorinated biphenyls on human liver cancer cells. While microplastics alone did not cause significant cell death, the combined exposure with PCBs produced distinct changes in cellular lipid profiles that differed from individual exposures. The study suggests that microplastics may alter how cells respond to co-occurring chemical pollutants through a "Trojan Horse" transport mechanism.
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.