Department of Chemistry, National Tsing Hua University, Hsinchu 30013, Taiwan.
Chemistry. 2010 Jul 19;16(27):8088-95. doi: 10.1002/chem.201000524.
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)H(8)N)(2) (1) (C(12)H(8)N=carbazolate) and the substitution ligands (S(2)CNMe(2))(2), SC(6)H(4)-o-NHC(O)(C(5)H(4)N) ((PyPepS)(2)), and P(C(6)H(3)-3-SiMe(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))(2)] (2) along with N-nitrosocarbazole (3). The subsequent nitrosation of N-acetylpenicillamine (NAP) by N-nitrosocarbazole (3) to produce S-nitroso-N-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.
（1）[(NO)(2)Fe(C(12)H(8)N)(2)]-（1）（C(12)H(8)N=carbazolate）与取代配体（S(2)CNMe(2))(2)、SC(6)H(4)-o-NHC(O)(C(5)H(4)N) ((PyPepS)(2))和 P(C(6)H(3)-3-SiMe(3)-2-SH)(3) ([P(SH)(3)]))反应，释放出不同的 NO 氧化还原相关形式（NO(+)、*NO 和 HNO/NO(-)）。
（2）与（PyPepS)(2)和 1 的 1:1 化学计量比反应形成 NO 自由基和配合物[PPN][Fe(PyPepS)(2)]（4）不同，进入的取代配体（S(2)CNMe(2))(2)触发了 1 向配合物[(NO)Fe(S(2)CNMe(2))(2)]（2）的转化，同时形成 N-亚硝基卡唑（3）。
（3）N-亚硝基卡唑（3）随后对 N-乙酰青霉胺（NAP）的亚硝化作用生成 S-亚硝基-N-乙酰青霉胺（SNAP），可能标志着通过 N-亚硝胺的转亚硝作用，DNIC 形成 S-亚硝硫醇的可能形成途径。
（4）[P(SH)(3)]对 1 的质子化作用引发 HNO 的释放和配合物[PPN][Fe(NO)P(C(6)H(3)-3-SiMe(3)-2-S)(3)]（5）的生成。
（5）同样，螯合配体 P(C(6)H(3)-3-SiMe(3)-2-SNa)(3) ([P(SNa)(3)])对 1 的亲核攻击直接释放了被((15)NO)Fe(SPh)(3)捕获的NO，从而生成((15)NO)((14)NO)Fe(SPh)(2)。
（6）这些结果说明了在配合物 1 与取代配体反应时，进入的取代配体（(S(2)CNMe(2))(2)与(PyPepS)(2)与[P(SH)(3)]/[P(SNa)(3)])与 DNIC 1 的咔唑配位配体如何协同作用，控制从 DNIC 1 释放 NO(+)、*NO 或NO。
（7）此外，这些结果表明，DNIC 可以作为 NO 在氧化还原信号过程中的中间物，通过向生物系统中不同的 NO 反应靶标提供不同的氧化还原相关形式的 NO 来发挥作用。
