Modification of Biochemical Properties of Nitrosothiol by [Fe.sup.3+] Cation: A Presumable Physiological Role

• Published in: Bulletin of experimental biology and medicine Vol. 168; no. 1; p. 41
• Main Authors: Titov, V.Yu, Osipov, A.N, Ibragimova, L.G, Petrov, V.A, Dolgorukova, A.M
• Format: Journal Article
• Language: English
• Published: Springer 22.03.2020
• Subjects: Ethylenediaminetetraacetic acid; Glycosylated hemoglobin; Iron compounds; Nitroso compounds; Physiological aspects; Thiols
• ISSN: 0007-4888; 1573-8221
• DOI: 10.1007/s10517-019-04641-7

In the presence of [Fe.sup.3+] cation, S-nitrosoglutathione (GSNO) loses the potency to inhibit catalase in the system containing hemoglobin (an NO trap) with iron chelator or -SH inhibitor (a "sulfhydric poison" [Hg.sup.2+]). In the absence of hemoglobin, the inhibitory potency is retained in both cases. These properties are characteristic of dinitrosyl-iron complexes containing ferrous iron and thiols (DNIC/RSH). Since the potency to inhibit catalase results from the presence of -NO group, its loss in the presence of hemoglobin relates probably to transfer of this group to hemoglobin. The nitrosothiols are relatively stable compounds, so their ability to release NO under the action of iron chelators, which is characteristic of DNIC/RSH, can have important physiological implications, because the role of such chelators can be played by some endogenous agents as well. Thus, release of NO from the donor compounds can be controlled and regulated. Probably, the agents such as nitrosothiol+[Fe.sup.3+] are the major constituents in the pool of nitroso compounds. Key Words: nitric oxide (NO); dinitrosyl-iron (II) complex with thiolate ligands (DNIC/RSH); S-nitrosoglutathione (GSNO); [Fe.sup.3+] cation