Why the study?
Despite ubiquitous detection in NO-producing cells, the chemical biology of dinitrosyl iron complexes remains only partially understood.
This review highlights the chemical biology of dinitrosyl iron complexes, emphasizing their formation mechanisms and roles in S-nitrosation and physiological processes.
DNICs may shape S-nitrosation in cardiovascular NO signaling; hypothesis-generating for mechanistic studies, clinical relevance remains open.
Dinitrosyl iron complexes (DNICs) are spontaneously and rapidly generated in cells. Their assembly requires nitric oxide (NO), biothiols, and nonheme iron, either labile iron or iron–sulfur clusters. Despite ubiquitous detection by electron paramagnetic resonance in NO-producing cells, the DNIC’s chemical biology remains only partially understood. In this Forum Article, we address the reaction mechanisms for endogenous DNIC formation, with a focus on a labile iron pool as the iron source. The capability of DNICs to promote S-nitrosation is discussed in terms of S -nitrosothiol generation associated with the formation and chemical reactivity of DNICs. We also highlight how elucidation of the chemical reactivity and the dynamics of DNICs combined with the development of detection/quantification methods can provide further information regarding their participation in physiological and pathological processes.
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Truzzi et al. (2021) studied this question.
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