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The evaluation to combined toxic effects of polypropylene microplastics and benzo[a]pyrene on macrophage cells
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Researchers exposed RAW264.7 macrophages to polypropylene microplastics combined with benzo[a]pyrene, finding that co-exposure enhanced cytotoxicity beyond BaP alone by suppressing antioxidant enzymes, elevating reactive oxygen species and malondialdehyde, and amplifying inflammatory IL-6 release, as confirmed by toxicoproteomic analysis.
Microplastics (MPs) pollution has emerged as a significant concern for human health, and their toxicological mechanisms help to better understand their potential risks. Previous studies paid main attention on the toxicity of MPs themselves, but in recent years, there has been growing awareness of their combined effects with other environmental pollutants. This study investigated the toxic effects of polypropylene microplastics (PP MPs) prepared via nonsolvent induced phase separation method in conjunction with benzo[a]pyrene (BaP) stimulation in vitro to macrophagocytes based on toxicoproteomics. We observed that PP MPs alone exhibited no obvious toxicity to the cells at concentrations of 50-150 μg/mL, while individual BaP induced significant cytotoxicity. Moreover, the combined exposure of PP MPs and BaP caused enhanced toxicity compared to BaP alone, where their combined exposure significantly suppressed the proliferation of RAW264.7 cells, exacerbated cell membrane damage, and increased apoptosis, resulting in substantial cellular toxicity. The possible toxic mechanisms were explored by measuring oxidative stress levels. It was found that co-exposure to PP MPs and BaP markedly inhibited superoxide dismutase (SOD) and catalase activities (CAT), reduced glutathione (GSH) level, elevated malondialdehyde (MDA) level, and increased intracellular reactive oxygen species (ROS) level compared to individual BaP exposure. Furthermore, proteomic analysis suggested that combined stimulation could lead to more serious oxidative damage, and further trigger intense inflammatory responses, validated by significant alterations in SOD, CAT, GSH, MDA, ROS, and IL-6. Therefore, this study provides new insights into assessing the risks associated with combined exposure to MPs and polycyclic aromatic hydrocarbons.
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Synergistic pulmonary toxicity of resorcinol bis(diphenylphosphate) and microplastics: Integrated proteomics and metabolomics approach reveals oxidative stress-inflammatory crosstalk
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Researchers exposed mice to the flame retardant resorcinol bis(diphenylphosphate) alone and in combination with polystyrene nanoplastics through inhalation. Using proteomics and metabolomics analysis, they found that co-exposure produced significantly worse lung damage than the flame retardant alone, through amplified oxidative stress and inflammatory signaling. The study reveals that nanoplastics can intensify the pulmonary toxicity of co-occurring environmental chemicals through synergistic mechanisms.
Combined toxicity and mechanisms of polystyrene nanoplastic co-exposed with bisphenol A/bisphenol AF in mouse macrophages RAW264.7
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Combined exposure of polystyrene microplastics and benzo[a]pyrene in rat: Study of the oxidative stress effects in the liver
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Researchers exposed rats to polystyrene microplastics and the carcinogen benzo[a]pyrene, both individually and in combination, to study oxidative stress in liver tissue. The combined exposure caused significantly more liver damage, inflammation, and oxidative stress than either pollutant alone. The study suggests that microplastics may amplify the harmful effects of environmental carcinogens when both are ingested together.
Repeated exposure to polyethylene microplastic mixtures containing PFAS and bisphenols activates THP-1 macrophages with inflammatory features
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Researchers exposed THP-1 macrophages repeatedly to polyethylene microplastics combined with PFAS and bisphenol additives to more accurately simulate real-world human contamination. The study found that repeated exposure activated macrophages with inflammatory features, suggesting that the combination of microplastics and their chemical additives may trigger immune responses in human cells.
Influence of polystyrene nanoparticles on the toxicity of tetrabromobisphenol A in human intestinal cell lines
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When human intestinal cells were exposed to both polystyrene nanoparticles and the flame retardant TBBPA together, the chemical pollutant dominated the toxic response, causing oxidative stress, DNA damage, and disruption of mitochondrial function. The study shows that mixing microplastics with other contaminants can produce complex, hard-to-predict health effects in gut cells, which matters because people are routinely exposed to multiple pollutants at once.
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