Fato Romana, Bergamini Christian, Leoni Serena, Lenaz Giorgio
Dipartimento di Biochimica G. Moruzzi, University of Bologna, 40126 Bologna, Italy.
Biofactors. 2008;32(1-4):31-9. doi: 10.1002/biof.5520320105.
Mitochondrial reactive oxygen species (ROS) are mainly produced by the respiratory chain enzymes. The sites for ROS production in mitochondrial respiratory chain are normally ascribed to the activity of Complex I and III. The presence of specific inhibitors modulates reactive oxygen species production in Complex I: inhibitors such as rotenone induce a strong ROS increase, while inhibitors such as stigmatellin prevent it. We have investigated the effect of hydrophilic quinones on Complex I ROS production in presence of different inhibitors. Some short chain quinones are Complex I inhibitors (CoQ2, idebenone and its derivatives), while CoQ1, decylubiquinone~ (DB) and duroquinone (DQ) are good electron acceptors from Complex I. Our results show that the ability of short chain quinones to induce an oxidative stress depends on the site of interaction with Complex I and on their physical-chemical characteristics. We can conclude that hydrophilic quinones may enhance oxidative stress by interaction with the electron escape sites on Complex I while more hydrophobic quinones can be reduced only at the physiological quinone reducing site without reacting with molecular oxygen.
线粒体活性氧（ROS）主要由呼吸链酶产生。线粒体呼吸链中ROS的产生位点通常归因于复合物I和III的活性。特定抑制剂的存在可调节复合物I中的活性氧产生：鱼藤酮等抑制剂会导致ROS大幅增加，而抑霉肽等抑制剂则可阻止这种情况。我们研究了亲水性醌类在不同抑制剂存在下对复合物I产生ROS的影响。一些短链醌类是复合物I抑制剂（辅酶Q2、艾地苯醌及其衍生物），而辅酶Q1、癸基泛醌（DB）和杜醌（DQ）是复合物I的良好电子受体。我们的结果表明，短链醌类诱导氧化应激的能力取决于与复合物I的相互作用位点及其物理化学特性。我们可以得出结论，亲水性醌类可能通过与复合物I上的电子逃逸位点相互作用来增强氧化应激，而疏水性更强的醌类只能在生理醌还原位点被还原，而不与分子氧反应。
