Fig. 5: NDUFA1 involvement in cisplatin-induced mitochondrial dysfunction and oxidative stress in tubular epithelial cell with IDH1-R132H mutation.

A Representative PI staining images depicting cisplatin-induced PTCs cell death isolated from Idh1^WT/WTKsp^Cre and Idh1^WT/MutKsp^Cre mice. Scale bar = 100 μm. B Quantification of cell death using PI/Hoechst staining and Image J software. C Overexpression of NDUFA1 alleviates cisplatin-induced mitochondrial dysfunction in renal tubular epithelial cells with IDH1-R132H mutation, as observed by Mito-tracker staining for mitochondrial morphology following cisplatin stimulation. Scale bar = 10 μm. Nuclei were counterstained with Hoechst. D MitoROS generation, ROS production and lipid ROS level of Idh1^WT/WT and Idh1^WT/Mut PTCs infected with a lentivirus encoding nothing (vector) or Flag-NDUFA1 was measured using MitoSOX, DCFH-DA and C11-BODIPY probe separately analyzed by FACS. E Representative PI staining images showing Ndufa1^+/+ and Ndufa1^−/− HK-2 cell death induced by cisplatin. Scale bar = 100 μm. F Quantification of cell death for using PI/Hoechst staining and Image J software. G Deletion of Ndufa1 exacerbates cisplatin-induced mitochondrial dysfunction in renal tubular epithelial cells, as observed by Mito-tracker staining for mitochondrial morphology following cisplatin stimulation. Scale bar = 10 μm. Nuclei were counterstained with Hoechst. H Deletion of Ndufa1 exacerbates cisplatin-induced renal tubular injury, as detected by MitoROS generation, ROS generation and lipid ROS levels using MitoSOX, DCFH-DA and C11-BODIPY probes in Ndufa1^+/+ and Ndufa1^−/− tubular cells.