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The microplastics exposure induce the kidney injury in mice revealed by RNA-seq
Summary
In a mouse study, microplastics of different sizes caused kidney injury including inflammation, oxidative stress, and scarring (fibrosis) after long-term exposure. The smallest particles (80 nanometers) altered immune-related genes, while larger particles disrupted genes tied to the body's internal clock. This research provides evidence that microplastics accumulating in the body over time could contribute to kidney disease in mammals, including humans.
Microplastics (MPs) may pollute drinking water, accumulate in the food chain, and release toxic chemicals that may cause a variety of diseases. The detrimental effects of MPs on kidney injury and fibrosis under long-term accumulation have not been fully documented. In this study, mice were exposed to MPs with three different diameters (80 nm, 0.5 µm, and 5 µm) to investigate the detrimental influences of MPs on the kidney. The results showed that MPs of different diameters caused varying degrees of injury to the murine kidney. MPs exposure can induce an inflammatory response, oxidative stress, and cell apoptosis in the kidney and induce kidney injury, which ultimately promotes kidney fibrosis. Furthermore, transcriptome data revealed that chronic exposure to MPs could alter the expressions of multiple genes related to immune response (80 nm) and circadian rhythm (0.5 µm, and 5 µm). Overall, our data provide new evidence and potential research for investigating the harm of MPs to kidney of mammals and even humans.
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