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Polystyrene nanoplastics exacerbate aflatoxin B1-induced hepatic injuries by modulating the gut−liver axis
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Mice exposed to both polystyrene nanoplastics and aflatoxin B1, a common food contaminant from mold, suffered worse liver damage than from either pollutant alone. The nanoplastics disrupted gut bacteria and weakened the intestinal barrier, allowing more toxins to reach the liver through the gut-liver axis. This study is concerning because it shows that microplastics can amplify the harmful effects of other food contaminants people are already exposed to.
Dietary pollution of Aflatoxin B1 (AFB1) poses a great threat to global food safety, which can result in serious hepatic injuries. Following the widespread use of plastic tableware, co-exposure to microplastics and AFB1 has dramatically increased. However, whether microplastics could exert synergistic effects with AFB1 and amplify its hepatotoxicity, and the underlying mechanisms are still unelucidated. Here, mice were orally exposed to 100 nm polystyrene nanoplastics (NPs) and AFB1 to investigate the influences of NPs on AFB1-induced hepatic injuries. We found that exposure to only NPs or AFB1 resulted in colonic inflammation and the impairment of the intestinal barrier, which was exacerbated by combined exposure to NPs and AFB1. Meanwhile, co-exposure to NPs exacerbated AFB1-induced dysbiosis of gut microbiota and remodeling of the fecal metabolome. Moreover, NPs and AFB1 co-exposure exhibited higher levels of systemic inflammatory factors compared to AFB1 exposure. Additionally, NPs co-exposure further exacerbated AFB1-induced hepatic fibrosis and inflammation, which could be associated with the overactivation of the TLR4/MyD88/NF-κB pathway. Notably, Spearman's correlation analysis revealed that the exacerbation of NPs co-exposure was closely associated with microbial dysbiosis. Furthermore, microbiota from NPs-exposed mice (NPs) partly reproduced the exacerbation of NPs on AFB1-induced systemic and hepatic inflammation, but not fibrosis. In summary, our findings indicate that gut microbiota could be involved in the exacerbation of NPs on AFB1-induced hepatic injuries, highlighting the health risks of NPs.
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Synergistic Toxicity of Combined Exposure to Acrylamide and Polystyrene Nanoplastics on the Gut–Liver Axis in Mice
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Researchers exposed mice to a combination of acrylamide, a common food processing byproduct, and polystyrene nanoplastics through drinking water and found that the combined exposure caused more severe gut and liver damage than either substance alone. The co-exposure disrupted gut barrier integrity, altered gut bacteria composition, and caused widespread metabolic changes. The study suggests that the interaction between nanoplastics and other food contaminants may amplify health risks beyond what each poses individually.
Gut–Liver Axis Mediates the Combined Hepatointestinal Toxicity of Triclosan and Polystyrene Microplastics in Mice: Implications for Human Co-Exposure Risks
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Mice co-exposed to the antimicrobial triclosan and polystyrene microplastics showed markedly worse intestinal and liver damage than those exposed to either contaminant alone, with gut microbiome disruption identified as a key mediating mechanism.
Combined toxicity of co-exposure to polystyrene nanoplastics and arsenic on the gut-liver axis in mice.
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Mice exposed to both nanoplastics and arsenic together, common pollutants that can show up in food and water, suffered worse gut and liver damage than expected, including a weakened gut barrier, disrupted gut bacteria, and increased inflammation. This suggests that real-world exposure to multiple pollutants at once may pose greater health risks than studying each one alone would predict.
Polystyrene microplastics exacerbated liver injury from cyclophosphamide in mice: Insight into gut microbiota
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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.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
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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.
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