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Adverse Effect of Polystyrene Nanoplastics in Impairing Glucose Metabolism in Liver Injury

International Journal of Molecular Sciences 2025 4 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Raden Joko Kuncoroningrat Susilo, Manikya Pramudya, Firli Rahmah Primula Dewi, Windy Seftiarini, Dewi Hidayati, Aunurohim Aunurohim, Aunurohim Aunurohim, Vuanghao Lim, Mochammad Aqilah Herdiansyah, Alfiah Hayati

Summary

Polystyrene nanoplastics disrupted glucose metabolism in liver cells by interfering with insulin signaling pathways and mitochondrial function, suggesting that nanoplastic exposure could contribute to metabolic disorders including insulin resistance.

Polymers
Body Systems
Study Type In vivo

Polystyrene nanoplastics (PS-NPs) are result from the degradation of plastic and have diameters ranging from 1 nm to 100 nm. The objective of this study is to provide information on the adverse effects of PS-NPs with in vitro and in vivo analyses of liver injury. An in vitro study was conducted using confocal microscopy, flow cytometry, and MTT test analysis. An in vivo study was conducted to determine apoptosis levels, glucose metabolism gene expressions, liver enzymes, and liver histology. Data were analyzed using GraphPad Prism software 10.2.1. The in vitro study showed the absorption of PS-NPs in the cell cytoplasm, the percentage of apoptosis, 3t3, and the WiDr cell lines' viability. The in vivo analysis showed that PS-NPs can stimulate liver injuries, such as inducing the elevation of liver enzymes, necrosis, edema, inflammation, and the dilatation of the portal vein diameter. High levels of caspase-3, caspase-9, and Bax were detected, as well as the expression of several genes including PI3K, AKT, PEPCK, GLUT2, and PK. In conclusion, the in vitro analysis showed the detrimental effects of PS-NPs on cells, such as high levels of apoptosis and low cell viability, while the in vivo studies displayed the impairment of liver tissue and disturbances in glucose metabolism regulation.

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