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The Combined Exposure to Polystyrene Nanoplastics and Bisphenol a Results in Mitochondrial Damage and Ferroptosis Via the Pi3k-Akt Signaling Pathway in the Kidneys of Mice

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Polymers
Body Systems
Models

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Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys

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Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.

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Cytotoxicity of Polystyrene Nanoplastics Involves Mitochondrial Dysfunction and DNA Damage in Hemocytes of the Pacific Oyster

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Scientists found that tiny plastic particles (nanoplastics) can damage the immune cells of oysters by harming their mitochondria, the "batteries" that power cells, leading to DNA damage even at low exposure levels. While this study was done in oysters, not humans, it adds to growing evidence that nanoplastics can disrupt basic cell functions, raising questions about what similar exposure might mean for human health given how widespread plastic pollution has become in our food and water.

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