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6:2 氯化多氟烷基醚磺酸盐(F-53B)诱导小鼠肾毒性,与氧化应激、炎症和纤维化相关。

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

作者信息

Wu Hua, Feng Yueying, Zhang Ruiying, Xu Hengyi, Fu Fen

机构信息

The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330000, China; State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, 330047, China.

State Key Laboratory of Food Science and Resources, Nanchang University, Nanchang, 330047, China.

出版信息

Chem Biol Interact. 2025 Jan 5;405:111290. doi: 10.1016/j.cbi.2024.111290. Epub 2024 Oct 22.

Abstract

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.

摘要

6:2 氯化聚氟烷基醚磺酸盐(商品名F-53B)是电镀行业中使用的全氟辛烷磺酸(PFOS)的替代品,已在一系列环境基质和生物体内被发现。它对哺乳动物具有多种生物毒性作用方式。肾脏对于维持体内平衡至关重要。然而,关于F-53B如何影响肾脏的研究却很少。在这项工作中,我们研究了长期口服F-53B对C57BL/6J小鼠的肾脏毒性。让小鼠自由饮用浓度为0、0.057、0.57和5.7毫克/升的F-53B,持续8周。在接触F-53B的小鼠中检测到肾脏氧化应激、炎症和纤维化,并且相关生化标志物的表达发生了显著改变。进一步研究表明,TGF-β1/Smad3和NF-κB信号通路可能与F-53B诱导的肾脏纤维化损伤和炎症有关。总体而言,本研究表明F-53B可能通过氧化应激,激活TGF-β1/Smad3和NF-κB信号通路导致肾脏损伤。这为进一步研究F-53B在哺乳动物中的有害机制提供了基础。

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