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Probing Long-Term Impacts: Low-Dose Polystyrene Nanoplastics Exacerbate Mitochondrial Health and Evoke Secondary Glycolysis via Repeated and Single Dosing
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This study exposed human intestinal cells to low doses of polystyrene nanoplastics over 12 days and found that repeated exposure caused cumulative damage to mitochondria, the energy-producing structures inside cells. Even concentrations considered environmentally realistic impaired cellular energy production and forced cells to switch to a less efficient backup energy system. This suggests that long-term, everyday nanoplastic exposure through food could gradually harm gut health in ways that might not be immediately noticeable.
Nanoplastics (NPs) are omnipresent in the environment and contribute to human exposure. However, little is known regarding the long-term effects of NPs on human health. In this study, human intestinal Caco-2 cells were exposed to polystyrene nanoplastics (nanoPS) in an environmentally relevant concentration range (102-109 particles/mL) under two realistic exposure scenarios. In the first scenario, cells were repeatedly exposed to nanoPS every 2 days for 12 days to study the long-term effects. In the second scenario, only nanoPS was added once and Caco-2 cells were cultured for 12 days to study the duration of the initial effects of NPs. Under repeated dosing, initial subtle effects on mitochondria induced by low concentrations would accrue over consistent exposure to nanoPS and finally lead to significant impairment of mitochondrial respiration, mitochondrial mass, and cell differentiation process at the end of prolonged exposure, accompanied by significantly increased glycolysis over the whole exposure period. Single dosing of nanoPS elicited transient effects on mitochondrial and glycolytic functions, as well as increased reactive oxygen species (ROS) production in the early phase of exposure, but the self-recovery capacity of cells mitigated these effects at intermediate culture times. Notably, secondary effects on glycolysis and ROS production were observed during the late culture period, while the cell differentiation process and mitochondrial mass were not affected at the end. These long-term effects are of crucial importance for comprehensively evaluating the health hazards arising from lifetime exposure to NPs, complementing the extensively observed acute effects associated with prevalent short-term exposure to high concentrations. Our study underlines the need to study the toxicity of NPs in realistic long-term exposure scenarios such as repeated dosing.
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Researchers exposed human intestinal cells to polystyrene nanoplastics over an extended period to simulate chronic dietary exposure. They found that long-term exposure at low concentrations caused subtle but persistent changes in cell function, including altered gene expression and increased oxidative stress markers. The study highlights that the health effects of nanoplastics may build up gradually over time, underscoring the importance of studying chronic rather than just short-term exposure.
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Scientists exposed human liver cells to tiny plastic particles (nanoplastics) at levels that didn't kill the cells, but found the cells' "power plants" (mitochondria) were already struggling—burning less fuel and producing less energy—along with other changes in how the cells process fat and nutrients. This matters because it suggests nanoplastics, which have already been found in real human liver tissue, may quietly stress liver cells and disrupt their metabolism even before any visible damage occurs, raising questions about long-term effects of everyday plastic exposure on liver health.
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