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20 resultsShowing papers similar to Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
ClearHepatic 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.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
Exposure to Polystyrene Microplastic Differentially Affects the Colon and Liver in Adult Male Mice
Researchers fed male mice polystyrene microplastics at varying doses for six weeks and examined the effects on their colon and liver. They found that the microplastics reduced antioxidant enzyme activity, damaged the intestinal barrier, disrupted mucus production, and caused tissue changes in both organs. The study provides further evidence that oral exposure to microplastics can cause oxidative stress and structural damage in the digestive system and liver.
Impact of the Oral Administration of Polystyrene Microplastics on Hepatic Lipid, Glucose, and Amino Acid Metabolism in C57BL/6Korl and C57BL/6-Lepem1hwl/Korl Mice
Researchers investigated the effects of orally administered polystyrene microplastics on liver metabolism in normal and obese mice over eight weeks. They found that microplastic exposure altered lipid, glucose, and amino acid metabolism pathways in the liver and adipose tissues. The study suggests that microplastic ingestion may disrupt hepatic metabolic functions, with potentially different impacts depending on baseline metabolic health status.
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.
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.
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 induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
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.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
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.
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.
Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.
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.
Assessment of the Toxicity of Polystyrene Microplastic in the Colon and Liver of Adult NMRI Mice
Researchers orally administered polystyrene microplastics to adult male mice at four doses for four weeks and examined histological changes in the colon and liver. Both organs showed dose-dependent tissue damage including inflammation and oxidative stress markers, with the colon showing earlier onset injury due to direct contact with ingested particles.
Comparative Analysisof Metabolic Dysfunctions Associatedwith Pristine and Aged Polyethylene Microplastic Exposure via theLiver-Gut Axis in Mice
Researchers fed mice low doses of pristine and aged polyethylene microplastics for several weeks and analyzed changes in blood metabolites, liver proteins, and gut bacteria. Both forms caused lipid metabolism disruptions and reduced beneficial gut bacteria, with aged microplastics showing greater toxicity linked to changes in fatty acid processing enzymes.