Effects of chlorfenapyr on nephrotoxicity under varying concentrations

This study investigates the nephrotoxic effects of varying concentrations of chlorfenapyr on Wistar rat kidneys and human kidney-2 (HK-2) cells. In vivo<i>,</i> chlorfenapyr at concentration of 30 mg/kg led to mild kidney tissue damage, as evidenced by hematoxylin and eosin (HE) and Masson's staining. Based on immunohistochemistry (IHC) results, chlorfenapyr also increased expression of fibrosis-related proteins. Flow cytometry showed decreased mitochondrial membrane potential (MMP) and increased apoptosis levels. These changes became more pronounced with increasing concentrations of chlorfenapyr. In vitro, HK-2 cells exposed to increasing chlorfenapyr concentrations exhibited elevated reactive oxygen species (ROS) levels, mitochondrial dysfunction, and apoptosis. Western blotting (WB) confirmed downregulation of mitochondrial markers Cytochrome c oxidase IV (COX IV), Translocase of Outer Mitochondrial Membrane 20 (TOM20), and Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), along with increased BCL2-Associated X (BAX) and decreased B-cell lymphoma-2 (Bcl-2) expression. Taken together, chlorfenapyr exhibits toxicity to both Wistar rat kidney tissues and HK2 cells, with its toxic effects increasing with higher concentrations.