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61,005 resultsShowing papers similar to Revealing transport, uptake and damage of polystyrene microplastics using a gut-liver-on-a-chip
ClearPolystyrene 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.
A digestive system microphysiological platform for assessment of internal-exposure risks and metabolic disease mechanisms induced by multi-size nano-plastics.
Researchers developed a digestive system organ-on-a-chip microphysiological platform to assess how nanoplastics (NPs) are absorbed, metabolized, and cause internal exposure risks. The system revealed size-dependent toxic effects of NPs on liver cells and lipid metabolism, providing mechanistic insights into NP-associated liver disease risk.
Environmentally Relevant Concentrations of Microplastic Exposure Cause Cholestasis and Bile Acid Metabolism Dysregulation through a Gut-Liver Loop in Mice
Mice exposed to environmentally realistic levels of polystyrene microplastics for 30 days developed damaged intestinal barriers, liver injury, and disrupted bile acid metabolism. The study revealed a gut-liver feedback loop where microplastics alter gut bacteria, which changes bile acid production, which in turn causes further liver damage, suggesting a mechanism by which everyday microplastic exposure could harm digestive health.
Microplastic-mediated new mechanism of liver damage: From the perspective of the gut-liver axis
This review describes how microplastics can damage the liver through the gut-liver axis: they first disrupt the gut's protective barrier and beneficial bacteria, allowing harmful substances to leak through the weakened intestinal wall into the bloodstream and travel to the liver. Once there, these substances cause inflammation, metabolic problems, and oxidative stress, offering a new explanation for how microplastic exposure could lead to liver disease.
Oral exposure to high concentrations of polystyrene microplastics alters the intestinal environment and metabolic outcomes in mice
In a mouse study, oral exposure to high concentrations of polystyrene microplastics caused fatty liver disease and abnormal blood lipid levels even without prior gut leakiness. The microplastics triggered intestinal inflammation through immune cells, disrupted gut bacteria, and altered how the body processes nutrients. These results suggest that swallowing microplastics could contribute to metabolic problems and liver disease in humans.
Polystyrene microplastics exposure: Disruption of intestinal barrier integrity and hepatic function in infant mice
Researchers found that even low concentrations of polystyrene microplastics caused significant gut barrier damage and liver injury in infant mice. The microplastics disrupted the intestinal lining, allowed particles to leak into the bloodstream, and triggered liver fat accumulation and altered gut bacteria colonization. The study raises concerns about microplastic exposure during early life, when developing digestive and liver systems may be especially vulnerable.
Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
Complex intestinal and hepatic in vitro barrier models reveal information on uptake and impact of micro-, submicro- and nanoplastics
Using laboratory models of human intestinal and liver barriers, researchers studied how plastic particles of different sizes cross from the gut into the body. Smaller nanoplastics (25 nm) were more readily taken up than larger microplastics, and the intestinal mucus layer provided some protection against particle absorption. The study also found signs of oxidative stress and changes in how liver cells process foreign substances after plastic exposure, providing insight into how ingested microplastics could affect human organs.
MRI-based microplastic tracking in vivo and targeted toxicity analysis
Researchers developed a new MRI-based method to track microplastics inside living mice over 21 days. They found that the liver was the primary organ where polystyrene microplastics accumulated, and this accumulation led to liver cell death, inflammation, and changes in enzyme levels. This tracking technique could help scientists better understand how microplastics move through and affect biological systems.
Microplastics in focus: a silent disruptor of liver health- a systematic review
This systematic review examines how micro- and nanoplastics affect liver health, based on 25 experimental and observational studies. The evidence shows that polystyrene particles can cause liver inflammation, oxidative stress, fat buildup, and disruption of metabolic pathways. These findings are concerning because the liver is the body's primary detoxification organ, and plastic-related damage could impair its ability to process other toxins.
Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis
Mice that drank water containing polystyrene microplastics for 13 weeks developed signs of obesity and metabolic dysfunction, with disruptions across the gut, liver, and fat tissue. The microplastics caused intestinal bacteria changes, liver inflammation, and altered fat storage, affecting the entire gut-liver-fat tissue communication system. These findings suggest that chronic microplastic ingestion through contaminated water and food could contribute to obesity and metabolic disease in humans.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Polystyrene microplastic exposure modulates gut microbiota and gut-liver axis in gilthead seabream (Sparus aurata)
Researchers fed gilthead seabream diets containing polystyrene microplastics and found that the particles disrupted the communication between the gut and liver, known as the gut-liver axis. The microplastics altered gut bacteria composition, increased liver inflammation markers, and changed bile acid metabolism. The study highlights how microplastic ingestion can trigger a chain of interconnected effects across multiple organ systems in fish.
Mitigation of polystyrene microplastic-induced hepatotoxicity in human hepatobiliary organoids through bile extraction
Using lab-grown human liver organoids, researchers discovered that polystyrene microplastics accumulate in bile ducts and cause liver cell damage. They found that a bile acid medication called ursodeoxycholic acid actually helped move microplastics into bile ducts for removal, while blocking bile transport made the liver damage worse. This study suggests that the body's bile system may play a role in clearing microplastics from the liver, pointing toward potential treatment strategies.
Disturbed Gut-Liver axis indicating oral exposure to polystyrene microplastic potentially increases the risk of insulin resistance
Researchers found that oral exposure to polystyrene microplastics in mice disrupted the gut-liver axis, causing intestinal inflammation and liver metabolic dysfunction that together increased the risk of insulin resistance. The study showed that microplastics damaged the intestinal barrier, allowing harmful substances to reach the liver and trigger metabolic disturbances. These findings suggest a potential pathway by which microplastic ingestion could contribute to metabolic health problems.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
Mechanisms of ingested polystyrene micro-nanoplastics (MNPs) uptake and translocation in an in vitro tri-culture small intestinal epithelium
Researchers used a sophisticated laboratory model of the human small intestine to study how micro- and nanoplastics cross the gut barrier after simulated digestion. They found that smaller nanoplastics were absorbed more efficiently than larger microplastics, and the particles used multiple cellular pathways to cross the intestinal lining. The study provides new evidence about the mechanisms by which ingested plastic particles could potentially reach the bloodstream.
[Exposure Pathways of Polystyrene Nanoplastics Mediate Their Cellular Distribution and Toxicity].
This study found that the route by which polystyrene nanoplastics enter the body determines which liver cell types accumulate the particles and what toxic effects occur, demonstrating that exposure pathway—not just dose—shapes nanoplastic toxicity in hepatic tissue.
Emerging threat of environmental microplastics: A comprehensive analysis of hepatic metabolic dysregulation and hepatocellular damage (Review)
This review summarizes existing research on how microplastics damage the liver, which is a key organ for filtering toxins from the body. Studies show that microplastics can cause liver tissue damage, trigger cell death, and disrupt fat metabolism, with smaller particles and longer exposure causing worse effects. The findings highlight the liver as a particularly vulnerable organ because it accumulates microplastics that enter the body through food and water.
Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.
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.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
Dose-effect of polystyrene microplastics on digestive toxicity in chickens (Gallus gallus): Multi-omics reveals critical role of gut-liver axis
Researchers fed chickens different doses of polystyrene microplastics and used multi-omics analysis to study digestive system damage through the gut-liver axis. They found that microplastics disrupted gut barrier function, altered liver metabolism, and changed gut bacterial communities in a dose-dependent manner. The study provides detailed molecular evidence of how microplastics can damage the digestive health of poultry, which may have implications for food safety.
Polystyrene microplastics exacerbated liver injury from cyclophosphamide in mice: Insight into gut microbiota
Researchers developed a mouse model to investigate whether chronic pre-exposure to polystyrene microplastics worsens liver injury caused by the drug cyclophosphamide. The study found that mice with 90 days of microplastic exposure showed significantly more severe liver damage when subsequently treated with cyclophosphamide, with changes linked to gut microbiota disruption. The findings suggest that chronic microplastic exposure may reduce the liver's resilience to additional chemical stressors.