Mitochondrial respiration and ROS production in chronically infected WT and PARP1^-/- mice.

<p>WT and PARP1^-/- mice were harvested at 150 days’ post-infection. <b>(A-D)</b> Cardiac myofiber bundles (~2 mg) were permeabilized, and mitochondrial respiratory function was measured using an Oxygraph-2k respirometer. After recording the state 4 respiration with addition of CI substrates (glutamate/pyruvate/malate), ADP was added, and state 3 respiration with electron input from complex CI was recorded (<b><i>A</i></b>). Rotenone (inhibits complex I) and CII substrate (succinate) were added to record CII-supported state 3 respiration (<b><i>B</i></b>). Competence of the outer mitochondrial membrane was assessed with addition of cytochrome c (<b><i>C</i></b>). The CII driven respiratory control ratio (RCR) is presented in <b><i>D</i></b>. <b>(E-G)</b> Isolated cardiac mitochondria were incubated in presence of CI (<b>E</b>) and CII (<b>F</b>) substrates, and the rate of H₂O₂ production was recorded. The total H₂O₂ levels in heart homogenates is shown in <b><i>G</i></b>. Data in all bar graphs are plotted as mean value ± SEM (n ≥ 5 mice/group, triplicate observations per sample). Statistical significance are marked as *WT.<i>Tc</i> vs. WT, ^&PARP1^-/-.<i>Tc</i> vs. PARP1^-/-, and ^#WT.<i>Tc</i> vs. PARP1^-/-.<i>Tc</i> (*^,&,#p<0.05, **^,##p<0.01).