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20 resultsShowing papers similar to Long-Term Exposure to Microplastics Promotes Early-Stage Hepatocarcinogenesis Induced by Diethylnitrosamine in Rats by Modulation of Their Gut Microbiota
ClearExposure to microplastics and liver oncogenesis: A comprehensive review on molecular mechanisms and pathogenic pathways
Researchers reviewed mechanisms by which microplastic exposure may promote liver cancer, identifying oxidative stress, mitochondrial dysfunction, inflammatory signaling, and epigenetic disruption as key pathways, while noting that microplastics can also carry heavy metals and organic pollutants that synergistically amplify hepatotoxic and carcinogenic risk.
Microplastics: An emerging environmental risk factor for gut microbiota dysbiosis and cancer development?
This review examines how microplastics may disrupt the gut microbiome and immune system in ways that could promote cancer development. Evidence from recent studies suggests microplastics can cause chronic inflammation, alter the balance of gut bacteria, and trigger molecular pathways linked to several cancer types including lung, liver, breast, and colon cancer. While more human research is needed, the review highlights a concerning connection between microplastic exposure, gut health, and cancer risk.
Microplastics exacerbate tissue damage and promote carcinogenesis following liver infection in mice
In a mouse study, microplastics significantly worsened liver damage during infection and activated cancer-related genetic pathways, including the tumor suppressor genes p53 and p21. Analysis of liver gene activity showed that microplastics intensified carcinogenesis pathways compared to infection alone, and big data analysis found a correlation between microplastic pollution and human liver cancer rates. While not proof of direct causation, this study raises the possibility that microplastic exposure could promote cancer development in damaged tissues.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.
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.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
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.
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.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis
This mouse study showed that polystyrene microplastics cause liver damage partly through disrupting gut bacteria, which then triggers harmful signals along the gut-liver connection. When researchers eliminated gut bacteria with antibiotics, liver damage from microplastics was reduced, confirming the gut microbiome plays a key role. Green tea extract (EGCG) helped protect the liver by restoring healthy gut bacteria, suggesting diet may help counteract some effects of microplastic exposure.
Microplastics: an often-overlooked issue in the transition from chronic inflammation to cancer
This review explores how microplastics that accumulate in the human body may trigger long-lasting inflammation, which is a known driver of cancer development. The authors describe how microplastics can disrupt the gut microbiome, activate immune responses, and alter signaling pathways in ways that could promote tumor growth over time.
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.
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.
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.
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.
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.
Long-term exposure to polystyrene microplastics promotes HFD-induced obesity in mice through exacerbating microbiota dysbiosis
Researchers found that long-term polystyrene microplastic exposure worsened high-fat-diet-induced obesity in mice by exacerbating gut microbiota dysbiosis, suggesting microplastic ingestion may amplify metabolic disease risk through disruption of the gut microbiome.
Integrated multi-omics of gut-liver axis to dissect the mechanism underlying hepatotoxicity induced by sub-chronic tire wear particles exposure in mice
Researchers gavaged female mice with tire wear particles (a major microplastic source) at three doses and performed integrated gut-liver multi-omics analysis, finding that sub-chronic exposure disrupted lipid metabolism, promoted liver inflammation, and altered gut microbial communities in a dose-dependent manner.
Gut microbiota and metabolic health risks from chronic low-dose microplastic exposure with focus on Desulfovibrio spp.
Researchers investigated the effects of long-term, low-dose polystyrene microplastic intake on gut bacteria and metabolism in mice. They found that even low doses significantly altered the gut microbiome, increasing bacteria linked to gastrointestinal inflammation and colorectal cancer risk, while also disrupting lipid and amino acid metabolism. The study suggests that routine microplastic exposure through food and water could quietly shift gut health in ways associated with chronic metabolic conditions.