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Microplastics and di (2-ethylhexyl) phthalate synergistically induce apoptosis in mouse pancreas through the GRP78/CHOP/Bcl-2 pathway activated by oxidative stress
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Researchers found that combined exposure to microplastics and the plasticizer DEHP synergistically induced pancreatic cell apoptosis in mice through oxidative stress activation of the GRP78/CHOP/Bcl-2 pathway, suggesting these co-occurring pollutants pose greater risk together than individually.
With the widespread use of plastics, microplastics (MPs) and di(2-ethylhexyl) phthalate (DEHP) have become emerging environmental pollutants. The combined toxicity of MPs and DEHP on the mouse pancreas and the specific mechanism of toxicity remain unclear. To establish in vitro and in vivo models to address these questions, mice were continuously exposed to 200 mg/kg/d DEHP and 10 mg/L MPs for 4 weeks. In vitro, MIN-6 cells were treated with 200 μg/mL MPs and 200 μM DEHP for 24 h. Based on toxicity assessed using CCK8 of the equivalent TU binary mixture, the IC50 of the TU-mix of DEHP and MPs 0.692 < 0.8, indicating a synergistic effect of the two toxicants. Meanwhile, our data revealed that compared to the control group, MPs and DEHP combined treatment increased ROS levels, inhibited the activity, and enhanced the expression of GRP78, and CHOP. Simultaneously, activated CHOP decreased the expression of Bcl-2, and increased the expression of Bax. In conclusion, DEHP and MPs synergistically induce oxidative stress, and activate the GRP78/CHOP/Bcl-2 pathway to induce pancreatic apoptosis in mice. Our finding provides a new direction for the research on the specific mechanism of MPs and DEHP combined toxicity.
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Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver
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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.
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Researchers investigated the combined toxic effects of the plasticizer DEHP and microplastics on liver cells in both mice and cell cultures. The study found that both substances individually caused oxidative stress, but their combined exposure significantly worsened the damage, leading to increased cell death through both apoptosis and necroptosis pathways. Evidence indicates that the antioxidant N-acetylcysteine could reverse these effects, confirming that oxidative stress is the key mechanism driving the liver damage.
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Researchers investigated how the plastic additive DEHP and polystyrene microplastics affect skeletal muscle in mice, finding that combined exposure caused more severe oxidative stress and cell death than either substance alone. The study suggests that co-exposure triggers apoptosis and necroptosis in muscle tissue by inhibiting a key cellular signaling pathway involved in cell survival.
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In mice, exposure to tiny plastic particles (nanoplastics) combined with a plastic chemical called DEHP caused more liver fat buildup and liver damage than either alone. Tests in liver cells showed this involved a specific stress pathway, and blocking that pathway reduced the fat buildup caused by the combined exposure.
Di (2-ethylhexyl) phthalate and polystyrene microplastics co-exposure caused oxidative stress to activate NF-κB/NLRP3 pathway aggravated pyroptosis and inflammation in mouse kidney
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When mice were exposed to both polystyrene microplastics and the plasticizer DEHP together, the kidney damage was significantly worse than from either pollutant alone. The combination triggered severe oxidative stress, activated inflammatory pathways, and caused a form of cell death called pyroptosis in kidney tissue. Since microplastics and DEHP frequently occur together in the environment, their combined impact on kidney health deserves serious attention.
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