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Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
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Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
Micro-nanoplastics (MNPs) are ubiquitously present in various natural habitats, and the kidney plays a critical role in eliminating metabolic waste from the body. Therefore, nephrotoxicity studies of MNPs are necessary. Consequently, we conducted a study utilizing a mouse model that underwent autonomous inhalation of polystyrene nanoplastics (PS-NPs) to investigate the impact of airborne nanoplastics (NPs) on kidney. The results demonstrated that airborne NPs could accumulate within the kidney subsequent to pulmonary entry. Transcriptome analysis showed that exposure to airborne NPs persistently interfered with important signaling pathways including oxidative stress, inflammation, and coagulation, which activated the NR4A1/CASP3 and TF/F12 signaling pathways. In vitro studies have shown that NPs were internalized by human kidney proximal tubular epithelial (HK-2) cells, leading to a range of pathological responses, and ultimately affecting cell fate. Furthermore, we pioneered the exposure of NPs to human kidney organoids. Our findings revealed a heightened sensitivity in kidney organoids towards NPs as compared to immortalized cell lines. This suggested that exposure to NPs could potentially inflict a more substantial toxic effect on the development of embryonic kidneys. In conclusion, this study has revealed the deleterious effects of exposure to airborne NPs on the mouse kidney.
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