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Combined exposure to di(2-ethylhexyl) phthalate and polystyrene microplastics induced renal autophagy through the ROS/AMPK/ULK1 pathway
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Researchers found that combined exposure to DEHP and polystyrene microplastics induced kidney autophagy through the ROS/AMPK/ULK1 pathway in mice and human kidney cells, with the combined effect being more severe than either pollutant alone.
Di(2-ethylhexyl) phthalate (DEHP) and polystyrene microplastics (PS-MPs) are new environmental pollutants that attracted increased attention. At present, the effects and underlying mechanisms of action of combined exposure of DEHP and PS-MPs on the kidney have not been elucidated. To investigate the renal toxicity of DEHP and PS-MPs exposure, we established single and combined DEHP and PS-MPs exposure models in mice and HEK293 cells, respectively. Hematoxylin and eosin staining, transmission electron microscopy, monodansylcadaverine staining, immunofluorescence, real-time quantitative PCR, Western blot analysis and other methods were used to detect relevant indicators. The results showed that the expression levels of ROS/AMPK/ULK1 and Ppargc1α/Mfn2 signaling pathway-related genes were significantly increased in the DEHP and PS-MPs exposure models. The mRNA and protein expression levels of autophagy markers were also upregulated. In addition, we found that the expression levels of mRNAs and proteins in the combined exposure group were more significantly increased than those in the single exposure group. In conclusion, combined exposure to DEHP and PS-MPs caused oxidative stress and activated the AMPK/ULK1 pathway, thereby inducing renal autophagy. Our results enhance the field of nephrotoxicity studies of plasticizers and microplastics and provide new light on combined toxicity studies of DEHP and PS-MPs.
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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.
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.
Coexposure to microplastic and Bisphenol A exhacerbates damage to human kidney proximal tubular cells
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This study exposed human kidney cells to polyethylene microplastics and bisphenol A (BPA, a common plastic chemical) together and found the combination was significantly more damaging than either substance alone. The co-exposure reduced cell survival and increased both oxidative stress and inflammation in the kidney cells. Since both microplastics and BPA are commonly found in the human body, their combined effect on kidney health is a real concern.
Di-(2-ethyl hexyl) phthalate induced oxidative stress promotes microplastics mediated apoptosis and necroptosis in mice skeletal muscle by inhibiting PI3K/AKT/mTOR pathway
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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.
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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