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Polystyrene microplastics modulation of hexavalent chromium toxicity in quails: transcriptomic and toxicological insights
Summary
Researchers exposed quails to both polystyrene microplastics and hexavalent chromium — a cancer-causing heavy metal — for 12 weeks, finding that microplastics worsened the kidney damage caused by chromium by disrupting fat metabolism and energy production. The combination triggered severe kidney scarring (fibrosis) that neither pollutant caused as strongly on its own, illustrating how microplastics can amplify the toxicity of other environmental contaminants.
Hexavalent chromium (Cr(VI)) is a globally recognized carcinogen that can lead to kidney toxicity. Microplastics (MPs) pollution is a serious environmental problem. The presence of Cr(VI) and MPs in the environment not only affects the ecological environment, but also impacts the health of humans and animals. Renal fibrosis represents a frequent final manifestation across a spectrum of chronic kidney conditions. This study aims to investigate whether chronic exposure to Cr(VI) and/or polystyrene (PS) promotes renal injury by altering fatty acid metabolism and energy metabolism, and inducing fibrotic responses. This study established a chronic co-exposure model in quails by simultaneously exposing them to Cr(VI) via drinking water and PS via oral gavage for 12 consecutive weeks. Experiments in vivo and transcriptome sequencing were performed to screen genes for analysis. The research results show that quails exposed to Cr(VI) and PS exhibited abnormal renal lipid and energy metabolism, leading to severe renal fibrosis. Overall, chronic exposure to PS exacerbates renal fibrosis process via promoting lipid dysregulation induced by Cr(VI) in quails. This study enriches the mechanism of nephrotoxicity induced by environmental PS-MPs and Cr(VI) contamination and contributes to the exploration of new preventive and therapeutic strategies. • Hexavalent chromium (Cr(VI)) and polystyrene (PS) have synergistic toxicity. • PS exacerbate Cr(VI)-induced nephrotoxicity in quails. • Cr(VI) induces renal lipid metabolism disorder by inhibiting fatty acid degradation. • PS aggravate Cr(VI)-induced renal energy metabolism disorders in quails. • PS enhance Cr(VI)-induced renal fibrosis in quails.
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