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. 2020 Apr 10;10(4):585. doi: 10.3390/biom10040585

Figure 7.

Figure 7

Deletion of VDAC1 impairs recovery of activities of complexes I and III of the electron transport chain in the renal cortex after ischemia-induced acute kidney injury. Activities of NADH:Ubiquinone Oxidoreductase (complex I) (a), Succinate:Ubiquinone Oxidoreductase (complex II) (b), and Ubiquinol:Cytochrome c Oxidoreductase (c) in mitochondria isolated from renal cortices of wild type (WT) and VDAC1-deficient (VDAC1 KO) mice on days 1 and 7 after bilateral renal ischemia (35 min). Protein levels (d) and densitometric analysis of immunoblots (e) of subunits NDUFA9, NDUFS3, NDUFB6, and NDUFS5 of NADH:ubiquinone oxidoreductase at different time points of recovery after bilateral renal ischemia (35 min) in wild type (WT) and VDAC1-deficient (VDAC1 KO) mice. Protein levels (f) and densitometric analysis of in immunoblots (g) of core protein 1 (cp1), core protein 2 (cp2), and Rieske subunit of ubiquinol:cytochrome c oxidoreductase at different time points of recovery after bilateral renal ischemia (35 min) in wild type (WT) and VDAC1-deficient (VDAC1 KO) mice. Results shown in (a–c) are the average ± S.E. of data obtained from five animals. * Values significantly different (p < 0.05) from respective WT sham-operated mice. # Values significantly different (p < 0.05) from respective VDAC1 KO sham-operated mice. The immunoblots (d,f) and their densitometric analysis (e,g) represent renal cortical mitochondria obtained from three sham-operated animals and three mice sacrificed on days 1 and 7 post reperfusion in three different experiments.