ABSTRACT
Since mitochondria are the main cellular source of reactive oxygen species, it is important to study the effect of dietary phenolic compounds on the level of ROS in these organelles. Using the EPR spectroscopy and TIRON probe, the ability of the investigated phenols (quercetin, rutin, caffeic acid, curcumin, and resveratrol) to scavenge superoxide anion radicals generated by isolated heart mitochondria of Wistar rats under variable oxygen partial pressure was studied. It was shown that during a 10 min incubation, caffeic acid in concentrations of 10-500 µM most effectively scavenged superoxide radicals formed in the complex III of the mitochondrial respiratory chain. A comparable antioxidant effect of rutin under these experimental conditions was observed at higher concentrations of 1-10 mM. The antioxidant activity of quercetin in the concentration range of 10-500 µM during the first minutes of incubation was higher than that of caffeic acid. Of the phenolic compounds studied, curcumin had the least effect on the superoxide radicals.
Subject(s)
Antioxidants/chemistry , Electron Spin Resonance Spectroscopy , Mitochondria, Heart/metabolism , Polyphenols/chemistry , Superoxides/chemistry , Animals , Curcumin/chemistry , Quercetin/chemistry , Rats , Rats, Wistar , Reactive Oxygen Species/chemistry , Reactive Oxygen Species/metabolism , Superoxides/metabolismABSTRACT
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. © 2018 BioFactors, 44(3):237-244, 2018.