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61,005 resultsShowing papers similar to Oral exposure to PLA microplastics induces time-dependent nanotoxicity via the gut-liver axis
ClearPolylactic acid micro/nanoplastic-induced hepatotoxicity: Investigating food and air sources via multi-omics
Researchers found that polylactic acid (PLA) — a plastic marketed as biodegradable — caused liver damage in mice whether the particles were ingested through food or inhaled through air, disrupting gut and lung microbiomes along the way. The findings challenge the assumption that biodegradable plastics are safe and suggest that micro- and nanoplastics from any source can pose a risk to liver health.
Hepatotoxicity induced by polylactic acid microplastics: The mediating role of gut microbiota and uric acid metabolism
Researchers found that polylactic acid (PLA) microplastics, often marketed as biodegradable and eco-friendly, caused liver damage in a study by disrupting gut bacteria and raising uric acid levels. The gut microbiome changes triggered by PLA microplastics were the key driver of the liver injury, not direct contact with the liver. This challenges the assumption that biodegradable plastics are safe and highlights the gut-liver connection in microplastic toxicity.
Continuous oral exposure to micro- and nanoplastics induced gut microbiota dysbiosis, intestinal barrier and immune dysfunction in adult mice
Researchers fed mice micro- and nanoplastics at environmentally relevant levels and found significant gut damage, including disrupted gut bacteria, weakened intestinal barriers, and reduced immune function. The ratio of beneficial to harmful gut bacteria shifted, and immune cells in the gut decreased. Importantly, the duration of exposure and the size of plastic particles mattered more than the amount consumed, suggesting even low-level long-term exposure could harm gut health.
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.
Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction
Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
This mouse study found that swallowing nanoplastics at levels found in the environment disrupted gut bacteria and damaged the intestinal barrier, allowing toxins to leak into the bloodstream and cause liver inflammation. When researchers transplanted gut bacteria from nanoplastic-exposed mice into healthy mice, those mice also developed liver damage. This demonstrates that nanoplastics may harm the liver indirectly by first disrupting the gut, a finding relevant to understanding how everyday plastic exposure could affect human health.
Insights into mouse metabolic health and gut microbiota responses to conventional and biodegradable microplastics released from plastic food containers
Researchers compared how conventional polyethylene and biodegradable polylactic acid microplastics from food containers affect mice over four weeks. They found that both types disrupted lipid metabolism and increased harmful gut bacteria, but the biodegradable PLA microplastics actually caused more severe metabolic disruption than conventional polyethylene. The study suggests that biodegradable plastics may not be safer than traditional plastics when it comes to microplastic exposure from food packaging.
In vivo exposure of mixed microplastic particles in mice and its impacts on the murine gut microbiome and metabolome
Mice were orally exposed to a mixed polystyrene, polyethylene, and PLGA microplastic suspension for several weeks and gut microbiome composition and metabolomics were analyzed. Mixed microplastic exposure shifted the gut microbiome toward dysbiotic profiles in both male and female mice, with accompanying metabolome changes related to lipid and amino acid metabolism.
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.
Oligomer nanoparticle release from polylactic acid plastics catalysed by gut enzymes triggers acute inflammation
Researchers found that polylactic acid (PLA), a popular 'eco-friendly' biodegradable plastic, releases nanoplastic particles when broken down by gut enzymes during digestion. In mice, these PLA fragments accumulated in the liver, intestine, and brain, causing intestinal damage and acute inflammation by interfering with a key immune enzyme, raising important questions about whether biodegradable plastics are truly safer for human health.
Unraveling the impact of micro- and nano-sized polymethyl methacrylate on gut microbiota and liver lipid metabolism: Insights from oral exposure studies
Mice that drank water containing tiny acrylic-type plastic particles (PMMA) for eight weeks developed liver damage, gut microbiome changes, and disrupted fat metabolism. The plastic particles accumulated in the liver and colon, triggering oxidative stress and activating pathways that increased cholesterol production. This study suggests that chronic exposure to even common plastic types through drinking water could harm liver health by disrupting the gut-liver connection.
Incorporation of polylactic acid microplastics into the carbon cycle as a carbon source to remodel the endogenous metabolism of the gut
Researchers discovered that gut bacteria can break down so-called biodegradable PLA microplastics and incorporate the carbon into their own metabolism, fundamentally altering the gut's energy balance. This process reduced beneficial short-chain fatty acids that fuel gut lining cells and caused decreased appetite and weight loss in mice, suggesting that biodegradable plastics may not be as harmless inside the body as assumed.
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.
Comparative Analysis of Metabolic Dysfunctions Associated with Pristine and Aged Polyethylene Microplastic Exposure via the Liver-Gut Axis in Mice
Mice fed both new and weathered polyethylene microplastics developed disrupted fat metabolism, liver oxidative stress, and shifts in gut bacteria, with weathered (aged) particles causing more severe effects. This study suggests that the microplastics people encounter in the real world, which have been degraded by sunlight and time, may be more harmful than the pristine particles typically used in lab studies.
Gut microbiota-mediated poly(ε-caprolactone) microplastic degradation exacerbates metabolic dysregulation
Researchers investigated the health effects of poly(epsilon-caprolactone), a biodegradable plastic commonly used in food packaging and medicine, and found that its microplastic form disrupted lipid metabolism and worsened metabolic problems in mice on a high-fat diet. They discovered that gut bacteria capable of breaking down this biodegradable plastic actually amplified its harmful metabolic effects. The study raises important questions about whether biodegradable plastics are truly safer than conventional plastics once they fragment into microplastics.
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.
Effects induced by polyethylene microplastics oral exposure on colon mucin release, inflammation, gut microflora composition and metabolism in mice
Researchers fed mice polyethylene microplastics for 30 days and found that even low doses reduced protective mucus in the colon, altered inflammation markers, and shifted the composition of gut bacteria. The microplastics increased the ratio of Bacteroides to Firmicutes bacteria and affected metabolic pathways in the gut microbiome. The study suggests that oral microplastic exposure may disrupt intestinal health by modifying the gut microbial community and its metabolism.
Oral exposure to polyethylene microplastics alters gut morphology, immune response, and microbiota composition in mice
Researchers fed mice polyethylene microplastics of two sizes commonly found in human stool for six weeks and examined the effects on gut health. The study found that microplastic exposure altered gut structure, disrupted immune cell function, changed gene expression related to inflammation and gut barrier integrity, and shifted the composition of gut bacteria. Mice exposed to both sizes simultaneously showed the most severe effects, suggesting that real-world exposure to mixed microplastic sizes may compound the damage.
Strain-Specific Toxicity of Polylactic Acid Biomicroplastics in Mice: Insights Into Liver and Intestine Responses
Researchers fed Swiss and C57Bl/6J female mice daily oral doses of polylactic acid biomicroplastics for 50 days and assessed liver and intestine responses. Despite equivalent exposure, the two mouse strains showed markedly different organ responses, highlighting that genetic background modulates susceptibility to bioplastic ingestion and cautioning against generalizing findings across populations.
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.
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.
Microbiota-mediated metabolic perturbations in the gut and brain of mice after microplastic exposure
In a mouse study, oral exposure to polystyrene microplastics of two sizes altered the gut bacteria community and caused metabolic changes in both the intestines and the brain. The disrupted gut bacteria appeared to drive changes in bile acid, energy, and other metabolic pathways. These findings support the idea that microplastics in food and water could affect brain health indirectly by first disrupting the gut microbiome and its chemical signals.
UnravelingPersistent Health Impacts in Mice FollowingCessation of Microplastic Exposure: Insights beyond the Surface
Mice were fed polystyrene microplastics (40-100 µm) at environmentally relevant or 10x doses for 21 weeks, then monitored for four weeks after exposure ceased. Despite stopping exposure, lipid metabolism disruption and gut microbiota dysbiosis persisted at high doses, indicating that microplastic-induced health impacts may not fully reverse after cessation.
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.