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. 2012 Jun 15;16(12):1421–1433. doi: 10.1089/ars.2011.4173

FIG. 1.

FIG. 1.

Complex I inhibitor rotenone leads to mitochondrial dysfunction, fragmentation, and enhanced reactive oxygen species (ROS) production. (A) Mitochondrial membrane potential (MMP; R123 mean fluorescence intensity [MFI] normalized on% of untreated control) and ATP levels were significantly reduced after 24-h treatment with rotenone (25 μM). (B) Levels of superoxide anion radicals (dihydroethidium [DHE] fluorescence normalized on% of untreated controls), and cytosolic ROS (dihydrorhodamin [DHR] fluorescence protein normalized on% of untreated controls) were increased after 2 h treatment with rotenone (25 μM). (C) Histogram of quantitative analysis of mitochondrial morphology (Mitotracker CMXRos) after 24 h rotenone insult (100 mitochondria/n). (D) Representative confocal images that revealed changes in the mitochondrial morphology of human embryonic kidney (HEK) cells treated with rotenone (25 μM, 24 h; bars represent 10 μm) compared to untreated controls after mitochondrial staining with MitoTracker CMXRos (red). (A–C) n=6±standard error of the mean (SEM); unpaired t-test; *p<0.05, **p<0.01, ***p<0.001. (To see this illustration in color the reader is referred to the web version of this article at www.liebertonline.com/ars).