Dinitrosyl iron complexes: Formation and antiradical action in heart mitochondria.

Mitochondria are widely known as a major source of reactive oxygen and nitrogen species for the cardiovascular system. Numerous studies established that superoxide anion radical production by heart mitochondria is only slightly suppressed under conditions of deep hypoxia, but is completely blocked under anoxia. It was found also that dinitrosyl iron complexes (DNIC) compare favourably with other physiologically active derivatives of nitric oxide (NO). DNIC with glutathione effectively scavenge superoxide radicals generated by mitochondria at different partial pressures of oxygen. Under conditions of simulated hypoxia, the synthesis of thiol-containing DNIC takes place in mitochondria and is concomitant with a significant decrease in the concentration of NO metabolites at the reoxygenation step. Free NO required for DNIC synthesis is generated in the reaction of S-nitrosothiols with superoxide or during single-electron oxidation of the nitroxyl radical (HNO) by coenzyme Q. Plausible mechanisms of antiradical effects of DNIC and their protective role in oxidative stress induced by hypoxia/reoxygenation of myocardial tissues are considered.