Executive Summary : | Nitric oxide (NO) and hydrogen sulfide (H₂S) are biologically relevant molecules with significant reactivity in various biological processes. NO plays a key role in blood pressure control, nerve signal transduction, and immune defense mechanisms in mammals. Some microbes, such as T. maritima, M. thermoacetica, and D. gigas, express the enzyme flavodiiron nitric oxide reductases (FNORs), which reduce NO to less toxic N₂O. FNORs have a nonheme diiron active site and a catalytic cycle that involves the formation of mono- and di-nitrosyl diiron(II) species. H₂S is recognized as a possible endogenous gasotransmitter with implications in physiological processes such as cardiovascular effects, vasodilation, cytoprotection, and neuromodulation. It may increase NO production and subsequent S-nitrosylation in endothelial cells, while its chemical interaction with NO may generate HNO. H₂S serves as an essential enhancer of vascular NO signaling and can modulate each other's enzymatic and non-enzymatic production. Understanding the mechanism of NO reduction by FNORs and the interaction of NO with H₂S/HS− in functional non-heme diiron complexes is of significant importance. This project proposes the synthesis, characterization, and detailed reactivity study of nitrosylated diiron complexes, investigating the role of hydrosulfide and related ligands during NO reduction and the mutual reactivity of iron, HS−, thiolates, and NO. Successful implementation of this project will significantly enhance existing knowledge regarding nitrosylated nonheme diiron-hydrosulfide complexes, their reactivity with reactive nitrogen species, reactivity towards N₂O generation, and the mutual reactivity of Fe(II), thiolate, NO, and HS− when combined in a controlled and sequential manner. |