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Combined BPA and DIBP Exposure Induced Intestinal Mucosal Barrier Impairment Through the Notch Pathway and Gut Microbiota Dysbiosis in Mice
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Researchers studied how two common plasticizers found in food packaging, BPA and DIBP, affect the gut when consumed together. They found that combined exposure caused more damage to the intestinal lining and disrupted beneficial gut bacteria in mice than either chemical alone. The study also identified a plant-based phenolic extract that helped counteract this intestinal damage, highlighting both the risks of plasticizer mixtures and potential natural protective strategies.
Bisphenol A (BPA) and diisobutyl (DIBP) phthalate are widely used as typical plasticizers in food packaging. Plasticizers can be released from polymers, migrate into food, and be ingested by humans, leading to various health problems. However, little research has investigated the combined toxicity of BPA and DIBP, particularly their intestinal toxicity. Our goal is to analyse the combined toxicity of BPA (50 mg/kg) and DIBP (500 mg/kg) on the intestines of KM mice. Additionally, we tried to find natural products that can inhibit or prevent the combined toxicity of BPA and DIBP. The results indicated that the combination of BPA and DIBP exposure resulted in a reduction of beneficial flora, an increase in D-Lac levels (136 ± 14 μmol/L), an increase in intestinal permeability, activation of the notch pathway, and a decline in intestinal stem cells (ISCs) to goblet cells, compared to single-exposure sources. Nevertheless, Rubus chingii Hu phenolic extract (RHPE) (200, 400 and 600 mg/kg) ameliorated the BPA and DIBP-induced intestinal microbiota disruption and intestinal mucosal barrier impairment by inhibiting the overactivation of the notch pathway. The results of this study highlight the potential risks to human health posed by the combination of BPA and DIBP and may help explain the potential pathways of enterotoxicity caused by combined ingestion.
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Researchers exposed mice to polystyrene nanoparticles and the plasticizer DEHP simultaneously, finding that co-exposure caused greater intestinal damage — including shorter villi, disrupted tight junctions, and reduced mucus coverage — than either contaminant alone, with gut microbiota alterations likely contributing to the enhanced toxicity.
Combined Enterohepatic Toxicity of Polystyrene Microplastics and Di(2-ethylhexyl) Phthalate in Mice: Gut Microbiota-Dependent Synergistic Effects
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Researchers investigated the combined toxicity of polystyrene microplastics and the plasticizer DEHP in mice, focusing on gut-liver axis effects. They found that co-exposure worsened harmful outcomes compared to either pollutant alone, with gut microbiota playing a key mediating role in the synergistic toxicity. The study suggests that microplastics and their associated chemical additives may interact to amplify health risks through disruption of the gut-liver connection.
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Mice exposed to both copper and microplastics together (a common combo, since copper pipes and plastic packaging both contaminate food and water) had more gut damage than mice exposed to either one alone — their intestinal lining weakened, "leaky gut" proteins dropped, and harmful gut bacteria increased while beneficial ones declined. This suggests that everyday combinations of environmental contaminants might harm gut health more than scientists get by studying pollutants one at a time, though more research is needed to confirm this applies to humans.
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Researchers studied the combined effects of polyethylene microplastics and the flame retardant TBBPA on human gut cells and gut bacteria in laboratory experiments. The study found that both substances damaged human intestinal cells, with TBBPA playing the larger role, while microplastics amplified certain harmful effects at high concentrations. TBBPA also selectively killed beneficial gut bacteria like Lactobacillus while promoting potentially harmful species, and microplastics enhanced this imbalance.
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Researchers exposed diabetic mice to polystyrene microplastics and bisphenol A, then examined intestinal effects using metabolomics and gut microbiome sequencing. The study found that both pollutants worsened intestinal injury in diabetic mice by disrupting gut barrier proteins, altering beneficial metabolites like long-chain fatty acids, and shifting gut microbial composition toward less favorable species.
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