摘要
Release of the distinct NO redox-interrelated forms (NO + , NO, and HNO/NO - ), derived from reaction of the dinitrosyl iron complex (DNIC) [(NO) 2 Fe(C 12 HaN) 2 ] - (1) (C 12 H 8 N = carbazolate) and the substitution Iigands (S 2 CNMe 2 ) 2 , [SC 6 H 4 -O-NHC(O)(C 5 H 4 N)] 2 , ((PyPepS) 2 ), and P(C 6 H 3 ,-3SiMe 3 -2-SH) 3 ([P(SH) 3 ]), respectively, was demonstrated. In contrast to the reaction of (PyPepS) 2 and DNIC 1 in a 1:1 stoichiometry that induces the release of an NO radical and the formation of complex [PPN][Fe(PyPepS) 2 ] (4), the incoming substitution ligand (S 2 CNMe 2 ) 2 triggered the transformation of DNIC 1 into complex [(NO)Fe(S 2 CNMe 2 J 2 ] (2) along with N-nitrosocarbazole (3). The subsequent nitrosation of N-acetylpenicillamine (NAP) by N-nitrosocarbazole (3) to produce S-nitroso-A-acetylpenicillamine (SNAP) may signify the possible formation pathway of S-nitrosothiols from DNICs by means of transnitrosation of N-nitrosamines. Protonation of DNIC 1 by [P(SH) 3 ] triggers the release of HNO and the generation of complex [PPN][Fe(NO)P(C 6 H 3 -3-SiMe 3 -2-S) 3 ] (5). In a similar fashion, the nucleophilic attack of the chelating ligand P(C 6 H 3 ,-3-SiMe 3 ,-2-SNa) 3 ([P(SNa) 3 ]) on DNIC 1 resulted in the direct release of [NO] - captured by [( 15 NO)Fe(SPh) 3 ] - , thus leading to [( 15 NO) - ( 14 NO)Fe(SPh) 2 ] - . These results illustrate one aspect of how the incoming substitution ligands ((S 2 CNMe 2 ) 2 vs. (PyPepS) 2 vs. [P(SH) 3 ]/[P(SNa) 3 ]) in cooperation with the carbazolate-coordinated ligands of DNIC 1 function to control the release of NO + , NO, or [NO] - from DNIC 1 upon reaction of complex 1 and the substitution ligands. Also, these results signify that DNICs may act as an intermediary of NO in the redox signaling processes by providing the distinct redox-interrelated forms of NO to interact with different NO-responsive targets in biological systems. © 2010 Wiley-VCH Verlag GmbH & Cu. KGaA.Weinheim.