Fig. 2.

Active suppression of respiration by the PHD O₂ sensor. A: neonatal cardiomyocytes were pretreated with DMSO (vehicle) or the PHI DMOG (250 μM) for 22 h before O₂ consumption measurements. 2,4-Dinitrophenol (DNP, 1 μM) was injected to measure uncoupled respiration. B: octanoic acid (OA) was added to standard glucose-containing buffer 35 min before injection of DNP. Values are means ± SE (n = 9). Every PHI-treated respiration value was significantly lower than corresponding vehicle control values (P < 0.05, by ANOVA followed by Bonferroni's post hoc analysis).