Skip to main content
. 2017 Aug 30;26(23):4541–4555. doi: 10.1093/hmg/ddx333

Figure 4.

Figure 4.

Effects of ROS scavenging on the high-salt dependent functional and ultrastructural impairment in mitochondria from SHRSR_KO Ndufc2 fibroblasts. (A,B) TMRM (A) and JC-1 (B) cytofluorimetric assay for mitochondrial membrane potential evaluation (Δψm). The pretreatment with resveratrol dampened the mitochondrial depolarization induced by high-salt stimulation (Student t test: *P < 0.05 vs unstimulated SHRSR_KO Ndufc2; ^P < 0.05 vs unstimulated SHRSR_KO Ndufc2 and P = NS vs salt stimulated SHRSR_KO Ndufc2; ^P < 0.05 vs unstimulated and salt stimulated SHRSR_KO Ndufc2). (C) Mito-SOX cytofluorimetric assay for mitochondrial ROS generation. The resveratrol counteracted the oxidative stress due to high-salt stimulation (Student t test: *P < 0.05 versus unstimulated SHRSR_KO Ndufc2; **P < 0.01 vs salt stimulated SHRSR_KO Ndufc2; see the pale grey area versus the grey line in the histogram) (D,E) Graphical representation of resveratrol treatment effects on the ultrastructural damage due to salt stimulation in SHRSR_KO Ndufc2 fibroblasts. The overall damage (Mt-G1 + 2+3) and the loss of inner cristae (IMM/OMM index) were lower in SHRSR_KO Ndufc2 fibroblasts treated with resveratrol compared with stimulated SHRSR_KO Ndufc2 (Kruskal-Wallis test in (D and E): **P < 0.05 vs salt stimulated SHRSR_KO Ndufc2). (F–I,L) Representative micrographs of mitochondria in high-NaCl exposed SHRSR_KO Ndufc2 fibroblasts, preatreated or not with resveratrol. After salt stimulus, the mitochondria from KO Ndufc2 fibroblasts showed a marked loss of cristae (F and G); in contrast, KO Ndufc2 fibroblasts pretreated with resveratrol (H, I and L) displayed organelles with a minor grade of damage. (TEM micrographs, uranyl acetate/lead citrate; Legend: Nu, nucleus; NM, nuclear membrane, PM, plasma membrane; rER, rough endoplasmic reticulum; IFb, intermediate filament bundles; Gx: grade of mitochondrial damage).