The mtDNA encodes for essential components of respiratory complexes and its deficiency can directly disturb the mitochondrial function. We, therefore, monitored if PARP1/PAR affect the OXPHOS capacity in chagasic myocardium. No significant differences in the basal level of mitochondrial respiration and state 4 respiration driven by CI or CII substrates were observed in the myocardial fibers of WT and PARP1-/- mice in presence or absence of chronic Tc infection. The CI and CII substrates driven ADP-coupled state 3 respiration (indicates proton gradient for ATP synthesis) as well as respiratory control ratio (RCR, state 3 / state 4) were maintained to normal levels in chronically infected PARP1-/- mice (Fig 4A, 4B and 4D). In comparison, we noted a 29% and 61% decline in CI- and CII-energized state 3 respiration, respectively (Fig 4A & 4B), and a 48% decline in CII-supported RCR (Fig 4D, all, p<0.05) in the myocardial fibers of WT.Tc (vs. WT) mice. Addition of cytochrome c did not improve the CII driven state 3 respiration in myocardial fibers of WT.Tc mice, thus, confirming that mitochondrial membranes were not damaged during experimental procedure (Fig 4C).