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Polystyrene Nanoplastics Chronic Exposure Aggravates Diabetic Kidney Injury in mice: role of mtROS/Sirt1 axis mediated renal tubular senescence
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In a study on diabetic mice, tiny plastic particles called nanoplastics (similar to those found in everyday plastic pollution) built up in the kidneys and made diabetes-related kidney damage worse by stressing out the cells' energy-producing mitochondria, causing kidney cells to age faster than normal. This matters because diabetic nephropathy already affects millions of people, and this research suggests that everyday exposure to plastic particles could be a hidden factor that speeds up kidney damage in an already vulnerable population, though more research is needed to confirm this happens in humans too.
Abstract Previous studies have suggested that polystyrene nanoplastics (PS-NPs) preferentially accumulate in the kidneys, posing a new threat to people with diabetic nephropathy. However, the adverse effect of chronic exposure of PS-NPs on diabetic kidney and underlying mechanisms remain largely unknown. Diabetic mice were orally administered PS-NPs (80 nm) at different doses (1, 10, and 50 mg/kg/day) for 60 days. PS-NPs was found mainly accumulated in the renal tubules rather than the glomeruli and caused tubular-specific damage as indicated by both pathological changes and increased levels of KIM-1/creatinine and NAG/creatinine in the urine. Mechanistically, the RNA-seq analysis of the kidney tissues of diabetic mice treated with PS-NPs revealed significant changes in mitochondrial-related genes.Co-localization of PS-NPs and mitochondria was detected in PS-NPs treated HK-2 cells, along with an increase in mtROS levels and a decrease in Sirt1 expression based on the experimental results from diabetic mice and HK-2 cells. Using the endocytosis inhibitor EIPA to inhibit the uptake of PS-NPs by HK-2 cells significantly reduced the mtROS levels within the cells. Furthermore, renal tubular senescence manifested by an increase in SA-β-galactosidase activity was further detected in both PS-NPs treated mice and HK-2 cells and that could be partially attenuated by the ROS inhibitor NAC.Overall, our study shows that PS-NPs mainly accumulate in the renal tubules rather than the glomeruli and can mediate the senescence of HK-2 cells by regulating the mtROS/Sirt1 axis.
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