Superoxide-mediated activation of uncoupling protein 2 causes pancreatic β cell dysfunction
J. Clin. Invest. Stefan Krauss, et al. 112:1831 doi:10.1172/JCI19774 [Go to this article.]

Figure 2
Effect of MnTBAP on proton leak, mitochondrial membrane potential, ATP, and oxygen consumption in intact thymocytes. (a and b) Proton leak in thymocytes. Thymocytes were incubated with oligomycin to block protons from re-entering the mitochondrial matrix via ATP synthase (top right points of each line). A submaximal concentration (80 nM) of the electron-transport chain inhibitor myxothiazol was added to reduce mitochondrial membrane potential to the resting-cell level (bottom left points in each line). Analyses were performed in thymocytes isolated from WT (a) and UCP2-deficient mice (b). Circles, control; squares, proton leak in the presence of MnTBAP (30 μM). Results are expressed as means ± SEM (n = 4–6). (c–e) Mitochondrial membrane potential, total cell ATP, and oxygen consumption were measured in resting thymocytes (no inhibitors added). White bars, control; black bars, 30 μM MnTBAP added. Cells were isolated from WT (left set of bars in each panel) and UCP2-deficient mice (right set of bars in each panel). Results are expressed as means ± SEM (n = 3–7). *P < 0.05, treated vs. untreated control; #P < 0.05, UCP2-deficient control vs. WT control.