Mitochondrial Complex I Inactivation After Ischemia-Reperfusion in the Stunned Heart

Nitric oxide provides myocardial protection when added to the cardiopulmonary bypass circuit during cardiac surgery: Randomized trial

“…5 In the hibernating myocardium, NO signaling induces neovascularization and improves functional reserve. 6,7 Correction of myocardial stunning occurs in patients with cardiac arrest administered with NO donors, improving cardiac function and cardiac output additionally to direct vasodilation of coronary arteries. 8 Proinflammatory cytokines are reduced in patients undergoing CABG treated with the NO donor sodium nitroprusside.…”

Xenobiotics Triggering Acute Intermittent Porphyria and Their Effect on Mouse Brain Respiratory Complexes

“…Previous studies attempting to explain the physiopathology of AIP have proposed that a reduction in the heme NOS cofactor could be involved [ 72 ]. NOS is also a modulator of the function of mitochondria through the interaction with Complex IV [ 66 ] and Complex I [ 71 , 72 ].…”

“…Previous studies attempting to explain the physiopathology of AIP have proposed that a reduction in the heme NOS cofactor could be involved [ 72 ]. NOS is also a modulator of the function of mitochondria through the interaction with Complex IV [ 66 ] and Complex I [ 71 , 72 ]. As it was mentioned previously, we described alterations in NOS activity and protein expression in the brains of CF1 mice with the administration of porphyrinogenic drugs depending on the drug analyzed [ 32 ].…”

Mitochondrial peroxynitrite generation is mainly driven by superoxide steady-state concentration rather than by nitric oxide steady-state concentration

“…Results from our laboratory have shown that even in physiopathological situations in which NO production is reduced, mitochondrial ONOOproduction rate may be slightly increased if the steady-state concentration of O 2 is augmented, with the consequent oxidation of biomolecules or modification of proteins by nitration. 61,65 We have observed that in myocardial stunning 61,65 and in streptozotocin (STZ)-induced diabetes, 62,39 the cardiac mitochondrial dysfunction implied the reduction in state 3 O 2 consumption sustained by glutamate-malate, the decrease in mitochondrial Complex I-III activity, and the enhancement in H 2 O 2 production rate (Table 1), among others. However, while in the mitochondrial dysfunction produced as a consequence of hyperglycemia, an increase in NO production rate (23%) and in mtNOS expression (132%) 39 were observed together with a reduction (50%) in Mn-SOD activity, in the mitochondrial impairment that accompanied the initial phase of stunned heart (15 min of ischemia and 30 min of reperfusion), a reduction in NO production rate (28%), without changes in mtNOS expression and SOD activity 61 were detected, as expected for an acute stress model.…”