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Chronic exposure to polystyrene microplastics increased the chemosensitivity of normal human liver cells via ABC transporter inhibition

The Science of The Total Environment 2023 19 citations

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Researchers found that chronic exposure to polystyrene microplastics made normal human liver cells more sensitive to certain chemotherapy drugs by inhibiting the cellular pumps that normally flush out toxic substances. This means the liver cells lost some of their natural defense mechanisms against chemical damage. The study suggests that long-term microplastic accumulation in the liver could alter how the organ processes medications and other foreign compounds.

Polymers
Body Systems

Microplastics (MPs) are ubiquitous in environmental compartments and consumer products. Although liver is frequently reported to be a target organ of MP accumulation in mammals, few studies have focused on MP hepatoxicity in humans. In this study, we used normal human liver cells, THLE-2, to assess the acute and chronic toxicity of polystyrene (PS) MPs with sizes of 0.1 and 1 μm. The results showed that after 48 h of exposure, both kinds of PS MPs could enter THLE-2 cells and cause no obviously acute cytotoxicity at <20 μg/mL. In contrast, metabolomic analysis revealed that 90 days of PS MPs exposure at environmentally relevant dose (0.2 μg/mL) could significantly alter the metabolic profiles of the cells, especially the nanosized MPs. KEGG pathway analysis showed that the ATP-binding cassette (ABC) transporter pathway was the most significantly changed pathway. Cell functional tests confirmed that chronic PS MP treatment could inhibit the activity of the ABC efflux transporter and further increase the cytotoxicity of arsenic, indicating that the PS MPs had a chemosensitizing effect. These findings underline the chronic risk of MPs to human liver.

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Polystyrene microplastics exacerbated liver injury from cyclophosphamide in mice: Insight into gut microbiota

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Researchers developed a mouse model to investigate whether chronic pre-exposure to polystyrene microplastics worsens liver injury caused by the drug cyclophosphamide. The study found that mice with 90 days of microplastic exposure showed significantly more severe liver damage when subsequently treated with cyclophosphamide, with changes linked to gut microbiota disruption. The findings suggest that chronic microplastic exposure may reduce the liver's resilience to additional chemical stressors.

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Researchers found that aged polystyrene nanoplastics can adsorb significantly more microcystin toxins than pristine nanoplastics, and the toxin-loaded particles caused greater harm to human liver cells. The combined exposure triggered metabolic energy disruption, oxidative damage, and stress in cellular machinery. The study suggests that environmentally weathered nanoplastics may pose amplified health risks by carrying higher loads of harmful waterborne toxins.

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Environmentally relevant UV-light weathering of polystyrene micro- and nanoplastics promotes hepatotoxicity in a human cell line

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Researchers found that UV-weathered polystyrene micro- and nanoplastics at environmentally relevant concentrations induced hepatotoxicity in human liver cells and caused significant changes in gene expression related to liver disease pathways.

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Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis

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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.

Article Tier 2

Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway

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This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.

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