N.N. Semenov Federal Research Center of Chemical Physics, Russian Academy of Sciences; Institute for Regenerative Medicine, I.M. Sechenov First Moscow State Medical University, Kosygin Str.4, Moscow, 119991, Russia.
Cell Biochem Biophys. 2019 Dec;77(4):279-292. doi: 10.1007/s12013-019-00886-1. Epub 2019 Oct 4.
Here, I present the data testifying that the conversion of free radical NO molecules to nitrosonium ions (NO), which are necessary for the realization of one of NO biological effects (S-nitrosation), may occur in living organisms after binding NO molecules to loosely bound iron (Fe ions) with the subsequent mutual one-electron oxidation-reduction of NO molecules (their disproportionation). Inclusion of thiol-containing substances as iron ligands into this process prevents hydrolysis of NO ions bound to iron thus providing the formation of stable dinitrosyl iron complexes (DNIC) with thiol ligands. Such complexes act in living organisms as donors of NO and NO, providing stabilization and transfer of these agents via the autocrine and paracrine pathways. Without loosely bound iron (labile iron pool) and thiols participating in the DNIC formation, NO functioning as one of universal regulators of diverse metabolic processes would be impossible.
在这里,我呈现的数据证明,自由态氮氧化物 (NO) 分子转化为亚硝酰阳离子 (NO+),这是实现 NO 生物学效应之一(S-亚硝化)所必需的,可能发生在生物体中,在将 NO 分子与松散结合的铁(Fe 离子)结合后,随后发生 NO 分子的相互单电子氧化还原(歧化)。将含巯基的物质作为铁配体纳入这一过程,防止与铁结合的 NO 离子水解,从而形成与巯基配体稳定的二硝酰基铁配合物(DNIC)。在生物体中,这些配合物作为 NO 和 NO 的供体,通过自分泌和旁分泌途径提供这些物质的稳定性和转移。如果没有松散结合的铁(不稳定铁池)和参与 DNIC 形成的巯基,NO 作为调节各种代谢过程的通用调节剂之一将是不可能的。