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Nanoplastics trigger the aging and inflammation of porcine kidney cells
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Researchers exposed pig kidney cells to nanoplastics in the laboratory and found that the particles were absorbed into cells in a time- and dose-dependent manner. The nanoplastics triggered oxidative stress, leading to a buildup of reactive oxygen species in mitochondria, which in turn caused inflammatory responses and premature cell aging. The findings provide new evidence that nanoplastic exposure may contribute to kidney cell damage through oxidative stress pathways.
Nanoplastics have now become a pervasive contaminant, being detected in various environmental media. However, our understanding of the specific toxicological effects of nanoplastics (NPs) on the kidneys remains unclear, which is a scientific problem that needs to be solved. To address this question, we employed two kidney cell lines as in vitro models to study the toxicological effects of NPs on porcine kidney cells. Firstly, we observed that NPs can be internalized into the cytoplasm in a time- and dose-dependent manner by using a laser confocal microscope. We further discovered that NPs can trigger inflammatory responses and lead to porcine kidney cell senescence by detection of senescence marker molecules. Furthermore, the potential molecular mechanism(s) by which NPs induce porcine kidney cell senescence were explored, we found that NPs induce oxidative stress in the porcine kidney cells, leading to the accumulation of reactive oxygen species (ROS) within mitochondria, ultimately triggering inflammatory responses and senescence in the kidney cells. In summary, our experimental results not only provide new evidence for the toxicity of NPs but also offer new ideas and directions for future research. This discovery will aid in our deeper understanding of the potential health impacts of NPs on domestic pigs.
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Researchers orally exposed Wistar rats to polystyrene nanoplastics at multiple doses for five weeks and observed dose-dependent increases in oxidative stress. The study found significant alterations in liver and kidney function markers, disrupted energy metabolism, and changes in antioxidant enzyme activity, suggesting that nanoplastic exposure may affect multiple organ systems in mammals.
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Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Polystyrene microplastics induce nephrotoxicity through impaired mitochondrial homeostasis: An integrated experimental study
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In an animal study, exposure to polystyrene microplastics built up in the kidneys and caused kidney damage, including harmful oxidative stress, inflammation, and disrupted function of mitochondria, the energy-producing parts of cells. Higher doses caused more buildup and more tissue damage, pointing to the kidney as a key target for microplastic harm.
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.
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This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
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