Batthyany Carlos, Schopfer Francisco J, Baker Paul R S, Durán Rosario, Baker Laura M S, Huang Yingying, Cerveñansky Carlos, Branchaud Bruce P, Freeman Bruce A
Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
J Biol Chem. 2006 Jul 21;281(29):20450-63. doi: 10.1074/jbc.M602814200. Epub 2006 May 8.
Nitric oxide ((*)NO)-derived reactive species nitrate unsaturated fatty acids, yielding nitroalkene derivatives, including the clinically abundant nitrated oleic and linoleic acids. The olefinic nitro group renders these derivatives electrophilic at the carbon beta to the nitro group, thus competent for Michael addition reactions with cysteine and histidine. By using chromatographic and mass spectrometric approaches, we characterized this reactivity by using in vitro reaction systems, and we demonstrated that nitroalkene-protein and GSH adducts are present in vivo under basal conditions in healthy human red cells. Nitro-linoleic acid (9-, 10-, 12-, and 13-nitro-9,12-octadecadienoic acids) (m/z 324.2) and nitro-oleic acid (9- and 10-nitro-9-octadecaenoic acids) (m/z 326.2) reacted with GSH (m/z 306.1), yielding adducts with m/z of 631.3 and 633.3, respectively. At physiological concentrations, nitroalkenes inhibited glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which contains a critical catalytic Cys (Cys-149). GAPDH inhibition displayed an IC(50) of approximately 3 microM for both nitroalkenes, an IC(50) equivalent to the potent thiol oxidant peroxynitrite (ONOO(-)) and an IC(50) 30-fold less than H(2)O(2), indicating that nitroalkenes are potent thiol-reactive species. Liquid chromatography-mass spectrometry analysis revealed covalent adducts between fatty acid nitroalkene derivatives and GAPDH, including at the catalytic Cys-149. Liquid chromatography-mass spectrometry-based proteomic analysis of human red cells confirmed that nitroalkenes readily undergo covalent, thiol-reversible post-translational modification of nucleophilic amino acids in GSH and GAPDH in vivo. The adduction of GAPDH and GSH by nitroalkenes significantly increased the hydrophobicity of these molecules, both inducing translocation to membranes and suggesting why these abundant derivatives had not been detected previously via traditional high pressure liquid chromatography analysis. The occurrence of these electrophilic nitroalkylation reactions in vivo indicates that this reversible post-translational protein modification represents a new pathway for redox regulation of enzyme function, cell signaling, and protein trafficking.
一氧化氮(·NO)衍生的活性物质使不饱和脂肪酸发生硝化反应,生成硝基烯烃衍生物,包括临床上大量存在的硝化油酸和亚油酸。烯烃硝基使这些衍生物在硝基的β位碳上具有亲电性,因此能够与半胱氨酸和组氨酸发生迈克尔加成反应。通过色谱和质谱方法,我们利用体外反应系统对这种反应活性进行了表征,并证明在健康人体红细胞的基础条件下,体内存在硝基烯烃 - 蛋白质和谷胱甘肽加合物。硝基亚油酸(9 -、10 -、12 - 和 13 - 硝基 - 9,12 - 十八碳二烯酸)(m/z 324.2)和硝基油酸(9 - 和 10 - 硝基 - 9 - 十八碳烯酸)(m/z 326.2)与谷胱甘肽(m/z 306.1)反应,分别生成 m/z 为 631.3 和 633.3 的加合物。在生理浓度下,硝基烯烃抑制甘油醛 - 3 - 磷酸脱氢酶(GAPDH),该酶含有一个关键的催化性半胱氨酸(Cys - 149)。两种硝基烯烃对 GAPDH 的抑制作用显示出约 3 μM 的半数抑制浓度(IC50),这一 IC50 与强效的硫醇氧化剂过氧亚硝酸盐(ONOO⁻)相当,但比过氧化氢的 IC50 低 30 倍,表明硝基烯烃是强效硫醇反应性物质。液相色谱 - 质谱分析揭示了脂肪酸硝基烯烃衍生物与 GAPDH 之间的共价加合物,包括在催化性 Cys - 149 处。基于液相色谱 - 质谱的人体红细胞蛋白质组分析证实,硝基烯烃在体内易于对谷胱甘肽和 GAPDH 中的亲核氨基酸进行共价、硫醇可逆的翻译后修饰。硝基烯烃对 GAPDH 和谷胱甘肽的加成显著增加了这些分子的疏水性,既诱导它们向膜的转运,也解释了为什么这些大量存在的衍生物以前通过传统的高压液相色谱分析未被检测到。体内这些亲电硝基烷基化反应的发生表明,这种可逆的翻译后蛋白质修饰代表了一种用于酶功能、细胞信号传导和蛋白质运输的氧化还原调节的新途径。