ИСТИНА

As early as 1972, Vakhnina and Ruuge showed that an EPR signal with a g-factor of 2.03 appears when nitrite is present in the mitochondria of the rat liver [1]. Thus, the formation of dinitrosyl iron complexes (DNIC) in mitochondria was recorded for the first time. We have established that S-nitrosothiols can also participate in the formation of DNIC in mitochondria from the heart of rats. The source of iron in the formation of these complexes can be iron-containing mitochondrial proteins [2]. The level of DNIC depends on the partial pressure of oxygen and the reactions, in which superoxide is produced by the mitochondrial respiratory chain. However, superoxide can stimulate the formation of DNIC. Conversely, it was shown that in various model systems containing DNIC with thiol ligands superoxide, alkoxy and alkyl peroxyl radicals were effectively scavenged. In addition, these complexes inhibit lipid peroxidation in mitochondrial membranes and low density lipoproteins. It has been found that the product of the single-electron reduction of nitric oxide – the nitroxyl anion (NO−) − can play an important role in the formation of DNIC with various ligands. The NO− is most effectively involved in the formation of DNIC associated with ergothioneine, carnosine and ADP. It is notable that in the presence of the donor of NO−, the carnosine-containing DNIC can be regenerated after destruction by ROS. The formation of nitrosylated hemoglobin (HbNO) in human erythrocytes is observed in the presence of NO donor diethylamine NONOate, whereas the contribution of DNIC with glutathione to this process is insignificant. It should be noted that HbNO is formed by the destruction of hemoglobin-associated DNIC under the action of superoxide [3], but not under the action of hypochlorous acid (HOCl). However, DNIC with glutathione effectively protect red blood cells from HOCl-induced hemolysis. In these experiments, phagocytic respiratory burst conditions were simulated. Earlier, it was found that DNIC are formed when generating activated macrophages [4]. The data obtained demonstrate that the formation of DNIC is important in protecting cells against oxidative stress.