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. 2022 Jun 16;13:887876. doi: 10.3389/fphar.2022.887876

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Copyright © 2022 Jiang, Hong and Fan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram illustrating the pharmacological, metabolic, and proteomic alterations in bismuth-treated proximal tubular cells. (A) HK-2 cells treated with CBS, and the bismuth ions were conjugated to GSH and transported to the vesicles, which can be exported by actin and the vesicle-tethering complex. The mechanism also sequesters cisplatin and likely other soft metal–based compounds. CBS downregulated the metabolism of amino acids and glycolysis but upregulated cystine importer Slc7a11. (B) GSH-depleted HK-2 cells treated with CBS, and the MT level was increased. CBS damaged intracellular protein and DNA, causing an increase of inclusion body, ubiquitin-mediated proteolysis, mismatch repair, and cytosolic DNA sensing mechanism. CBS also affects the mitochondrial respirasome.