# Antioxidant Action of Dinitrosyl Iron Complexes in Model Systems Containing Cytochrome c and Organic Hydroperoxides

## TL;DR

This study explores how dinitrosyl iron complexes (DNICs) act as antioxidants in systems involving cytochrome c and hydroperoxides, potentially preventing oxidative stress and apoptosis.

## Contribution

The study reveals that DNICs with glutathione ligands are more effective antioxidants than glutathione alone in model mitochondrial systems.

## Key findings

- DNICs with glutathione and phosphate ligands reduced prooxidant levels in reaction systems with cytochrome c and cumene hydroperoxide.
- DNICs-GS intercepted free radicals and prevented cytochrome c oligomerization induced by hydroperoxides.
- Reduced glutathione was less effective as an antioxidant and sometimes showed prooxidant properties.

## 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.