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Co-Exposure to Polystyrene Microplastics and Bisphenol A Contributes to the Formation of Liver Fibrosis in Mice through Inhibition of the BMAL1/E-Cad Signaling Pathway
Summary
Researchers found that co-exposure to polystyrene microplastics and bisphenol A caused liver fibrosis in mice by disrupting a key signaling pathway that controls cell adhesion. The combined exposure produced more severe liver damage than either substance alone, with excessive buildup of scar tissue in the liver. The study suggests that the widespread co-occurrence of microplastics and BPA in food packaging could pose synergistic risks to liver health.
The food safety risks posed by exposure to polystyrene microplastics (PS-MPs) and bisphenol A (BPA) have become an issue worldwide. However, the toxic effects of PS-MPs and BPA coexposure on the mammalian liver remain elusive. In this study, we found that PS-MPs and BPA coexposure have synergistic toxic effects on AML12 cells and the mouse liver. Histopathological staining revealed excessive accumulation of the extracellular matrix in the coexposure liver. Co-exposure to PS-MPs and BPA downregulated Bmal1 and E-cad both in vitro and in vivo. Additionally, Bmal1-/- AML12 cells and liver-specific Bmal1-/- mice exhibited significantly reduced E-cad levels, with no significant reduction under PS-MPs and BPA coexposure. Notably, overexpression of BMAL1 and CLOCK significantly enhanced luciferase activity driven by the E-cad gene intron region (containing an E-box cis-element). These results demonstrated that coexposure to PS-MPs and BPA contributed to the development of liver fibrosis by inhibiting the BMAL1/E-cad signaling pathway.
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