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61,005 resultsShowing papers similar to In vivo hepatic effects and post-exposure recovery following polyethylene terephthalate microplastic ingestion in Swiss Albino mice ( Mus musculus )
ClearIn vivo hepatic effects and post-exposure recovery following polyethylene terephthalate microplastic ingestion in Swiss Albino mice (Mus musculus)
Researchers exposed Swiss Albino mice to two concentrations of PET microplastics for 14 days via drinking water, finding significant liver enzyme disruption and oxidative stress markers, followed by a 7-day depuration period that showed partial recovery of some but not all biomarkers.
In vivo hepatic effects and post-exposure recovery following polyethylene terephthalate microplastic ingestion in Swiss Albino mice (Mus musculus)
This in vivo study found that ingesting PET microplastics at 1 and 2 mg/mL for 14 days caused significant liver toxicity in mice—including disrupted ALT, catalase, and SOD enzyme activity—with partial but incomplete recovery after a 7-day depuration period.
Chronic PET‐Microplastic Exposure: Disruption of Gut–Liver Homeostasis and Risk of Hepatic Steatosis
Researchers exposed mice to PET microplastics ground from plastic bottles over 29 weeks and found that the particles caused obesity, liver enlargement, fatty liver disease, and early-stage scarring of liver tissue. The microplastics also disrupted gut bacteria and bile acid metabolism, pointing to damage along the gut-liver connection. The findings raise concerns about the long-term health effects of chronic exposure to the type of microplastics commonly found in food and beverages.
Renal and Hepatotoxic Effects of Polyethylene Terephthalate Microplastics in Chronically Exposed Albino Rats
Researchers exposed albino rats to different doses of PET microplastics for 90 days and measured kidney and liver function markers. They found that chronic exposure led to significant changes in serum urea, creatinine, and liver enzymes, suggesting potential kidney and liver damage at higher doses. The study also found that water stored in PET containers exposed to sunlight showed similar toxic effects, raising concerns about everyday plastic container use.
Evaluation of Liver Function Through SGOT and SGPT Quantification in Rats Administered Polyethylene Terephthalate Microplastics
Researchers administered PET microplastics orally to white rats at doses of 0.4–1.0 mg/day and measured SGOT and SGPT liver enzyme levels, finding dose-dependent increases in both transaminases indicating hepatotoxicity even at low exposure levels.
Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice
Researchers found that mice exposed to PET microplastics (the type commonly found in plastic bottles) over 17 weeks developed liver damage, including fat buildup, oxidative stress, and cell death. The study revealed that the damage was driven by changes in gut bacteria that altered lipid metabolism, and when researchers depleted the gut bacteria, the liver damage was reduced. This suggests the gut microbiome plays a key role in how microplastics cause harm to internal organs.
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.
Exploring the Impacts of Polyethylene Microplastics on Rat Liver
Wistar rats exposed to polyethylene microplastics at 0.1–5 mg/kg for 4 weeks showed dose-dependent PE accumulation in liver tissue confirmed by fluorescence microscopy, with histopathological signs of liver injury despite no significant change in body weight.
Polyethylene terephthalate microplastics affect gut microbiota distribution and intestinal damage in mice
Mice exposed to PET microplastics, the type commonly found in plastic bottles, developed intestinal inflammation, changes in gut bacteria, and signs of a weakened gut barrier. Even at relatively low doses, the microplastics increased liver stress markers and disrupted the protective mucus layer in the colon, suggesting that everyday PET plastic exposure could contribute to digestive health problems.
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.
PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study
Researchers fed immature piglets PET microplastics for four weeks and examined the effects on their livers. They found that microplastic exposure altered gene expression patterns related to metabolism and immune response, and increased markers of oxidative stress in the liver. The study suggests that even relatively short-term microplastic ingestion may disrupt liver function at the molecular level.
Potential Impact Microplastic Polyethylene Terephthalate on Mice
Researchers studied how polyethylene terephthalate (PET) microplastics affect mice when ingested, tracking where the particles end up in the body. They found that microplastics accumulated in various organs and caused measurable biological effects. The study adds to growing evidence that common plastic types found in food packaging may pose health risks when consumed.
Dysbiosis of gut microbiota in C57BL/6-Lepem1hwl/Korl mice during microplastics-caused hepatic metabolism disruption
Researchers administered polypropylene microplastics orally to obese mice for 9 weeks and found disruption of hepatic lipid, glucose, and amino acid metabolism alongside structural changes in gut microbiota, with microplastic-treated mice showing decreased hepatic lipid accumulation and altered abundance of specific bacterial genera.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers exposed adult male mice to polyethylene microplastics on normal or Western diet for 90 days, examining synergistic effects between plastic and dietary stress on gut and liver health. Microplastic exposure disrupted gut barrier integrity, altered the microbiome, and affected liver homeostasis, with some effects differing between normal and Western diet groups.
In vivo test of acute exposure of polyethylene microplastics on kidney and liver of Rattus norvegicus Wistar strain rats
Researchers exposed male rats to a single dose of polyethylene microplastics and monitored them for 14 days, finding significant changes in body weight, elevated markers of kidney and liver stress in blood tests, and visible tissue abnormalities under microscopy. The results indicate that even short-term, high-dose microplastic exposure can cause measurable organ damage in mammals.
Organ-specific accumulation and toxicity analysis of orally administered polyethylene terephthalate microplastics
When mice were fed tiny PET plastic particles (the kind found in water bottles and food containers), the particles accumulated mainly in the lungs and caused inflammatory damage at higher doses. The study found that male mice were more sensitive than females, and the results highlight that microplastics swallowed through food and drink can travel to and harm organs beyond the digestive system.
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.
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.
Chronic Microplastic Exposure Dose‐Dependently Induces Liver Failure via Oxidative Stress, Inflammation, and Apoptosis in Rats
This animal study found that chronic exposure to polyethylene microplastics caused dose-dependent liver damage in rats over just four weeks. Higher doses led to increased markers of liver injury, oxidative stress, inflammation, and cell death, suggesting that ongoing microplastic ingestion could harm liver health over time.
Acute Toxicity Assessment of Orally Administered Microplastic Particles in Adult Male Wistar Rats
Researchers gave adult male rats a single oral dose of microplastics made from PET water bottles and found that even this one-time exposure altered markers of liver, heart, and kidney function. Higher doses also reduced food intake and increased signs of oxidative stress, which is cell damage caused by harmful molecules. This study suggests that even brief microplastic exposure could trigger early changes in organ function, raising questions about the cumulative effect of daily human exposure through food and water.
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.
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.
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.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers orally exposed adult male mice to polyethylene microplastics under both normal and high-fat diets, assessing effects on the gastrointestinal tract. The study found that diet influences microplastic-induced gut changes, with greater effects observed in animals fed a western-style high-fat diet.