Figure 1.

Effects of prenatal hypoxia and nMitoQ treatment on cardiac mitochondrial respiration in young adult male offspring. Oxidative phosphorylation (OXPHOS) capacity for the (A) Reduced nicotinamide adenine dinucleotide (NADH) pathway (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) male offspring exposed to prenatal hypoxia (blue) or normoxia (red) after treatment with saline (closed symbols) or nMitoQ (open symbols). 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.