Figure 5.
Mitochondrial respiration of permeabilized muscle fibers from the cardiac septum of control fetuses, and fetuses in the CORT, DCA, and CORT + DCA groups. Oxygen consumption (O2 flux) is reported as integrative mitochondrial function (per tissue weight, pmol·s−1·mg wet wt−1) and as intrinsic mitochondrial function (per mitochondrial unit, with weight-specific citrate synthase activity as a proxy for mitochondrial content; pmol·s−1·U CS activity−1) in the following respiratory states: LEAK respiration, activated respiration supported by complex I substrates (OXPHOS, PCI), activated respiration supported by complex I and II substrates (OXPHOS, PCI+II), maximal respiration (maximal ETS capacity, ECI+II), ETS capacity with only complex II substrates (ECII), and maximal electron transport capacity of complex IV (ECIV; with TMPD as the electron donor in the presence of ascorbate; for concentrations of all substrates, inhibitors, and uncoupler, see text. Leak, PCI, PCI+II, ECI+II, and ECII are corrected for residual, nonmitochondrial oxygen consumption (ROX), whereas ECIV is corrected for chemical background. Values are means ± SE; n = 7 control, 6 CORT, 6 control + DCA, and 5 CORT + DCA samples of septum. aMain effect of DCA treatment at P < 0.05. CORT, cortisol-infused; DCA, dichloroacetate; ETS, electron transport system; TMPS, N,N,N′,N′-tetramethyl-p-phenylenediamine.