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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Cell Metab. 2009 Mar;9(3):265–276. doi: 10.1016/j.cmet.2009.01.012

Fig. 5. Physiological role of the intramitochondrial mito-sAC pathway in the regulation of OXPHOS and ROS production.

Fig. 5

A) COX Vmax in mouse liver mitochondria with CAI (n=9), CAI plus HCO3− (n=9) and CAI plus 8Br-cAMP (n=9) and pyruvate and malate as substrates. CAI decreased COX activity, which was rescued by HCO3− or 8Br-cAMP. AA (n=6), blocked CO2-production by the TCA cycle and decreased COX activity, which was rescued by HCO3− or 8Br-cAMP. B) cAMP levels in mitochondria decreased when CA or the TCA cycle were blocked with CAI and AA, respectively. HCO3− reverted the effects of CAI or AA (n=8). C) CAI (n=6) decreased respiration in HeLa cells and this inhibition was prevented by 8Br-cAMP (n=3). Control, untreated cells (n=33). D) Respiration in cells grown in glucose or galactose medium (black bars) (n=6) for 48 hours. The calcium ionophore A23187 (dashed bars) increased respiration in control (untreated) cells in glucose. E) ROS production in cells grown in glucose or galactose and treated as in D (n=6). Galactose resulted in decreased ROS production in control cells (black bars). All other comparisons are between treated and untreated cells grown under the same conditions (i.e., glucose or galactose medium). *, p<0.05; **, p<0.001; ***, p<0.0001.