Abstract
The antioxidant/prooxidant effects of dinitrosyl iron complexes (DNICs), physiological donors of nitric oxide (NO(•)), are studied in reaction systems modeling processes with cytochrome c occurring in mitochondria under oxidative stress and leading to apoptosis. Using luminol-dependent chemiluminescence, DNICs with glutathione and phosphate ligands were shown to decrease the level of prooxidants in a reaction system containing ferricytochrome c and cumene hydroperoxide. Electron paramagnetic resonance (EPR) spectroscopy revealed that glutathione DNICs (DNICs-GS) intercepted the free radicals formed during the interaction between cytochrome c and tert-butyl hydroperoxide. DNICs-GS were also shown to prevent the formation of oligomeric forms of cytochrome c, which were induced by organic hydroperoxides. Reduced glutathione was less effective as an antioxidant than DNICs-GS or could even occasionally exhibit the prooxidant properties. Ferricytochrome c also catalyzed the formation of DNICs-GS with nitroxyl anion (NO(-)) taking part.