Coenzyme Q10 and related quinones oxidize H2S to polysulfides and thiosulfate
Coenzyme Q10 and related quinones oxidize H2S to polysulfides and thiosulfate
复制标题
DOI：
10.1016/j.freeradbiomed.2022.02.018
复制
发表时间：
2022-03-01
影响因子：
7.4
通讯作者：
Straub, Karl D.
中科院分区：
文献类型：
--
作者：
Olson, Kenneth R.;Clear, Kasey J.;Straub, Karl D.
在线粒体 H2S 氧化的经典途径中，电子通过泛醌 (CoQ(10)) 从硫化物：醌氧化还原酶 (SQR) 转移到复合物 III。我们之前观察到许多醌直接氧化 H2S，我们假设 CoQ(10) 可能具有类似的性质。在这里，我们使用 H2S 和多硫化物荧光团（AzMC 和 SSP4）、银纳米粒子来测量硫代硫酸盐 (H2S2O3)、质谱法来识别多硫化物和 O-2 敏感光极来测量 O-2 消耗，在缓冲液中检查 CoQ(10) 和更亲水的截短形式 CoQ(1) 和 CoQ(0) 对 H2S 的氧化。我们表明，所有三种醌浓度依赖性地催化缓冲液中 H2S 氧化为多硫化物和硫代硫酸盐，其效力为 CoQ(0)> CoQ(1)> CoQ(10)，并且 CoQ(0) 特异性地将 H2S 氧化为全多硫化物 H2S2,3,4。这些反应消耗并需要氧气，并且通过添加 SOD 来增强，这表明氧化 H2S 的是醌，而不是超氧化物。相关醌、MitoQ、甲萘醌和艾地苯醌在类似的反应中氧化 H2S。外源性 CoQ(0) 减少细胞 H2S 并增加多硫化物和硫代硫酸盐的产生，这也是 O-2 依赖性的，表明醌对细胞中的硫代谢具有类似的作用。总的来说，这些结果表明了 H2S 代谢的另一种内源性机制以及 H2S 相关代谢紊乱的潜在治疗方法。
In the canonical pathway for mitochondrial H2S oxidation electrons are transferred from sulfide:quinone oxidoreductase (SQR) to complex III via ubiquinone (CoQ(10)). We previously observed that a number of quinones directly oxidize H2S and we hypothesize that CoQ(10) may have similar properties. Here we examine H2S oxidation by CoQ(10) and more hydrophilic, truncated forms, CoQ(1) and CoQ(0), in buffer using H2S and polysulfide fluorophores (AzMC and SSP4), silver nanoparticles to measure thiosulfate (H2S2O3), mass spectrometry to identify polysulfides and O-2-sensitive optodes to measure O-2 consumption. We show that all three quinones concentration-dependently catalyze the oxidization of H2S to polysulfides and thiosulfate in buffer with the potency CoQ(0)> CoQ(1)> CoQ(10) and that CoQ(0) specifically oxidizes H2S to per-polysulfides, H2S2,3,4. These re-actions consume and require oxygen and are augmented by addition of SOD suggesting that the quinones, not superoxide, oxidize H2S. Related quinones, MitoQ, menadione and idebenone, oxidize H2S in similar reactions. Exogenous CoQ(0) decreases cellular H2S and increases polysulfides and thiosulfate production and this is also O-2- dependent, suggesting that the quinone has similar effects on sulfur metabolism in cells. Collectively, these results suggest an additional endogenous mechanism for H2S metabolism and a potential therapeutic approach in H2S-related metabolic disorders.