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Impact of Plastic-Related Compounds on P-Glycoprotein and Breast Cancer Resistance Protein In Vitro
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Researchers examined how plastic-related compounds affect P-glycoprotein and breast cancer resistance protein in vitro, finding that plasticizers and plastic additives can inhibit these critical cellular defense transporters involved in detoxification.
Plastic in oceans degrades to microplastics and nanoplastics, causing various problems for marine fauna and flora. Recently, microplastic has been detected in blood, breast milk and placenta, underlining their ability to enter the human body with still unknown effects. In addition, plastic contains other compounds such as plasticizers, antioxidants or lubricants, whose impact on human health is also elusive. On the cellular level, two transporters involved in cell protection and detoxification of xenobiotic compounds are the ABC-transporters P-glycoprotein (P-gp, MDR1, ABCB1) and breast cancer resistance protein (BCRP, ABCG2). Despite the great importance of these proteins to maintain the correct cellular balance, their interaction with plastic and related products is evasive. In this study, the possible interaction between different plastic-related compounds and these two transporters was investigated. Applying virtual compound screening and molecular docking of more than 1000 commercially available plastic compounds, we identified candidates most probably interacting with these two transporters. Cytotoxicity and uptake assays confirmed their toxic interaction on P-glycoprotein-overexpressing CEM/ADR5000 and BCRP-overexpressing MDA-MD-231-BCRP cell lines. To specifically visualize the results obtained on the P-glycoprotein inhibitor 2,2'-methylenebis(6-tert-butyl-4-methylphenol), we performed live cell time-lapse microscopy. Confocal fluorescence microscopy was used to understand the behavior of the molecule and the consequences that it has on the uptake of the well-known substrate doxorubicin and, in comparison, with the known inhibitor verapamil. Based on the results, we provide evidence that the compound in question is an inhibitor of the P-glycoprotein. Moreover, it is also possible that 2,2'-methylenebis(6-tert-butyl-4-methylphenol), together with three other compounds, may also inhibit the breast cancer resistance protein. This discovery implies that plastic-related compounds can not only harm the human body but can also inhibit detoxifying efflux pumps, which increases their toxic potential as these transporters lose their physiological functions.
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Chemicals added to plastics, like those found in food packaging and everyday products, can interfere with proteins in our cells that normally control how drugs and hormones move in and out of our bodies. This review pulls together existing research showing these interactions happen even at the low levels most people are exposed to daily, which could affect how our bodies process both medications and these plastic-derived chemicals. More research is needed, but this matters because it suggests everyday plastic exposure might have subtle effects on drug effectiveness and hormone balance that scientists don't yet fully understand.
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This review examines how bisphenols, chemical compounds widely found in plastic consumer products, may interact with the GPER-1 receptor to promote breast cancer cell proliferation. Researchers highlight that bisphenol A and related compounds can act as endocrine disruptors, underscoring concerns about widespread human exposure to plastic-derived chemicals.
Polystyrene Microplastics Disrupt Anticancer Proteins: An In Silico and In Vitro Study
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Molecular docking and cell culture experiments showed that polystyrene microplastics act as competitive inhibitors of melatonin receptors MT1 and MT2 — proteins central to anticancer signaling — and bind strongly to complement immune regulators Factor H and Factor I, while also inducing cytotoxicity and apoptosis in colon and breast cancer cell lines. These findings suggest microplastic exposure may interfere with the body's own cancer-suppression and immune regulatory mechanisms at the molecular level.
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Researchers reviewed how co-exposure to nanoplastics and heavy metals produces synergistic toxicity across multiple species and cell models, finding that nanoplastics enhance metal bioavailability and amplify oxidative stress, mitochondrial dysfunction, apoptosis, and gut dysbiosis more severely than equivalent microplastic co-exposures.
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Researchers studied how common industrial pollutants called PFAS chemicals interact with nanoplastics and blood proteins in the human body. The study found that when nanoplastics are present, they actually reduce the cellular uptake of PFAS chemicals and lessen their toxicity, because the protein layer that forms on nanoplastic surfaces traps the pollutants and limits their availability to cells.
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