6:2 chlorinated polyfluoroalkyl ether sulfonate (F–53B) induced nephrotoxicity associated with oxidative stress, inflammation and fibrosis in mice

• Published in: Chemico-biological interactions Vol. 405; p. 111290
• Main Authors: Wu, Hua, Feng, Yueying, Zhang, Ruiying, Xu, Hengyi, Fu, Fen
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 22.10.2024
• Subjects: F-53B; Fibrosis; Inflammation; Nephrotoxicity; Oxidative stress; TGF-β1/Smad3 signaling pathway; Oxidative stress; F-53B; Inflammation; TGF-β1/Smad3 signaling pathway; Nephrotoxicity; Fibrosis; fibrosis; nephrotoxicity; inflammation; oxidative stress
• ISSN: 0009-2797; 1872-7786; 1872-7786
• DOI: 10.1016/j.cbi.2024.111290

6:2 Chlorinated polyfluoroalkyl ether sulfonate (trade name F–53B) is a substitute for perfluorooctane sulfonate (PFOS) used in the plating industry, and has been found in a range of environmental matrices and livings. There are numerous ways by which it is biotoxic to mammals. The kidneys are critical for maintaining homeostasis. However, little research has been conducted on how F–53B affects the kidneys. In this work, we investigated the renal toxicity of long-term oral F–53B treatment in C57BL/6J mice. Mice were allowed to drink F–53B freely at concentrations of 0, 0.057, 0.57, and 5.7 mg/L for 8 weeks. Renal oxidative stress, inflammation, and fibrosis were detected in mice exposed to F–53B, and the expression of related biochemical markers was significantly altered. Further investigations revealed that the TGF-β1/Smad3 and NF-κB signaling pathways may be associated with F–53B-induced renal fibrotic damage and inflammation. Overall, this study suggested that F–53B causes renal injury possibly via oxidative stress, activating the TGF-β1/Smad3 and NF-κB signaling pathways. This provides a foundation for further research into the harmful mechanism of F–53B in mammals. [Display omitted] •F–53B exposure induces kidney injury in mice.•F–53B exposure-induced nephrotoxicity in mice is associated with oxidative stress and inflammation.•F–53B exposure activates TGF-β1/Smads signaling pathways to induce renal fibrosis.