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Long-Term Exposure to Microplastics Promotes Early-Stage Hepatocarcinogenesis Induced by Diethylnitrosamine in Rats by Modulation of Their Gut Microbiota
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Using a long-term mouse exposure model, researchers found that chronic microplastic ingestion promoted early-stage liver cancer development through oxidative stress, inflammation, and epigenetic alterations, providing mechanistic evidence for a microplastics-hepatocarcinogenesis link.
Hepatocarcinogenesis is linked to environmental factors, with microplastics (MPs) emerging as a global environmental concern that may contribute to liver injury. However, the impact of MPs on the early stages of hepatocarcinogenesis has been largely ignored. Here we investigated the impact of long-term MP exposure on the formation of preneoplastic lesions during hepatocarcinogenesis induced by diethylnitrosamine (DEN) in rats. Rats were injected with DEN to induce preneoplastic lesions, and then they were orally administered with 1 µm MPs 0.5 mg/kg body weight per day for 20 weeks. The results revealed that long-term exposure to MPs did not induce the formation of glutathione S-transferase placental form (GST-P)-positive foci as preneoplastic lesions during hepatocarcinogenesis in these animals, thereby indicating non-carcinogenicity. However, MP exposure resulted in a 1-fold increase in both the number and size of GST-P-positive foci in rats initiated with DEN compared to those treated with DEN alone. Accordingly, MP exposure led to a 0.61-fold increase in the index of proliferating cell nuclear antigen (PCNA)-positive cells in DEN-initiated rats when compared to DEN treatment alone. In addition, the composition of the gut microbiota was significantly altered, accompanied by various levels of short-chain fatty acids. Our results suggest that long-term MP exposure can promote pre-neoplastic lesion formation in DEN-induced rats by increased cell proliferation as well as alterations in the gut microbiota and short-chain fatty acid levels. This highlights the potential health risks associated with hepatocarcinogenesis linked to long-term exposure to MPs.
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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?
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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
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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.
Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut–Liver Axis
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In mice, polystyrene microplastics caused liver inflammation and fibrosis and disturbed the gut microbiome. Wiping out gut bacteria with antibiotics reduced the inflammation but not the fibrosis, and transplanting microbiota from exposed mice reproduced the inflammation. Mice given EGCG, the main polyphenol in green tea, had less liver injury.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
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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.
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