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. 2014 May 13;3:e02242. doi: 10.7554/eLife.02242

Figure 1. Metformin inhibits mitochondrial complex I function.

(A) Relative mitochondrial oxygen consumption rate (OCR) of intact Control-HCT 116 p53−/− and (B) NDI1-HCT 116 p53−/− cells treated with metformin in complete media for 24 hr. (C) Relative complex I (2 mM malate, 10 mM pyruvate, 10 mM ADP)-driven oxygen consumption rate of saponin permeabilized Control-HCT 116 p53−/− cells and (D) NDI1-HCT 116 p53−/− cells treated with metformin for 20 min in mitochondrial assay buffer. (E) Relative complex II-driven oxygen consumption rate of saponin permeabilized Control-HCT 116 p53−/− cells treated with 10 mM succinate and 10 mM ADP in the presence of 1 mM metformin or the complex II inhibitor 3-Nitropropionic acid (3-NPA). (F) Representative western blot and quantification of levels of OCT1 protein in Control BFP-HCT 116 p53−/− and NDI1-HCT 116 p53−/− cells. Error bars are SEM (OCR: n = 4; OCT1: n = 4). * indicate significance p<0.05.

DOI: http://dx.doi.org/10.7554/eLife.02242.003

Figure 1.

Figure 1—figure supplement 1. NDI1 expression slightly increases oxygen consumption.

Figure 1—figure supplement 1.

(A) Basal mitochondrial oxygen consumption rate of Control-HCT 116 p53−/− (+BFP) and NDI1-HCT 116 p53−/− cells normalized to Control-HCT 116 p53−/− cells. (B) Coupled mitochondrial oxygen consumption rate of Control-HCT 116 p53−/− and NDI1-HCT 116 p53−/− cells normalized to Control-HCT 116 p53−/− cells.
DOI: http://dx.doi.org/10.7554/eLife.02242.004