Altered Mitochondrial Respiration and Other Features of Mitochondrial Function in Parkin-Mutant Fibroblasts from Parkinson’s Disease Patients

Figure 1

Respiratory flux profiles of patient-derived and control fibroblasts, as determined by a Seahorse Extracellular Flux Analyzer with twelve consecutive measurements of oxygen consumption rate (OCR). Addition of ATP synthase inhibitor oligomycin, electron transport chain uncoupler FCCP and complex I and III inhibitors rotenone and antimycin A are indicated. (a) Respiratory flux profiles of patient-derived and control fibroblasts. Results are expressed as mean ± SEM. (b) Illutrative respiratory flux profile indicating various parameters of respiratory control. These include: OCR due to non-mitochondrial respiration (rotenone/antimycin A response); basal mitochondrial OCR (basal measurement minus rotenone/antimycin A response); ATP-linked OCR (basal measurement minus oligomycin response); OCR due to proton leak (oligomycin response minus rotenone/antimycin A response); ATP coupling efficiency (basal mitochondrial OCR divided by ATP-linked OCR); maximum OCR (FCCP response minus rotenone/antimycin A response) and spare respiratory capacity (maximum OCR divided by basal mitochondrial OCR). AU, arbitrary units; Ct, control; OCR, oxygen consumption rate; P, patient; SEM, standard error of the mean.

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