Figure 2.

Effects of prenatal hypoxia and nMitoQ treatment on cardiac mitochondrial respiration in young adult female offspring. Oxidative phosphorylation (OXPHOS) capacity for the (A) NADH (N-) pathway (substrates pyruvate, malate, and glutamate generating NADH, which feed electrons into complex I), (B) NADH- and succinate- (NS) pathways (maximum OXPHOS capacity when both NADH- and succinate- pathways are active), (C) succinate (S-) pathway (succinate feeding electrons into complex II after rotenone-mediated complex I inhibition), and (D) complex IV activity (ascorbate and TMPD feeding electrons into complex IV) were measured in the hearts of young adult (4-month-old) female offspring exposed to prenatal hypoxia (blue) or normoxia (red) after treatment with saline (closed symbols) or nMitoQ (open symbols). Outlier data points are shown in gray. O₂ flux is measured as [pmol/(s*mg)] where * stands for multiplication. Data were presented as mean ± SEM (n = 8–12 dams/group, 1–2 offspring/dam/group) and analyzed by two-way ANOVA with an unpaired two-tailed t post hoc test and Bonferroni correction (* p < 0.05, ** p < 0.01).