Noack H, Kube U, Augustin W
Institut für Pathobiochemie, Medizinische Akademie Magdeburg, F.R.G.
Free Radic Res. 1994 Jun;20(6):375-86. doi: 10.3109/10715769409145637.
In order to evaluate different mitochondrial antioxidant systems, the depletion of alpha-tocopherol and the levels of the reduced and oxidized forms of CoQ were measured in rat liver mitochondria during Fe++/ascorbate and NADPH/ADP/Fe++ induced lipid peroxidation. During the induction phase of malondialdehyde formation, alpha-tocopherol declined moderately to about 80% of initial contents, whereas the total CoQ pool remained nearly unchanged, but reduced CoQ9 continuously declined. At the start of massive malondialdehyde formation, CoQ9 reaches its fully oxidized state. At the same time alpha-tocopherol starts to decline steeply, but never becomes fully exhausted in both experimental systems. Evidently the oxidation of the CoQ9 pool constitutes a prerequisite for the onset of massive lipid peroxidation in mitochondria and for the subsequent depletion of alpha-tocopherol. Trapping of the GSH by addition of dinitrochlorbenzene (a substrate of the GSH transferase), results in a moderate acceleration of lipid peroxidation, but alpha-tocopherol and ubiquinol levels remained unchanged when compared with the controls. Addition of succinate to GSH depleted mitochondria effectively suppressed MDA formation as well as alpha-tocopherol and ubiquinol depletion. The data support the assumption that the protective effect of respiratory substrates against lipid peroxidation in the absence of mitochondrial GSH is mediated by the regeneration of the lipid soluble antioxidants CoQ and alpha-tocopherol.
为了评估不同的线粒体抗氧化系统，在铁离子/抗坏血酸和NADPH/ADP/铁离子诱导的大鼠肝脏线粒体脂质过氧化过程中，测定了α-生育酚的消耗以及辅酶Q还原型和氧化型的水平。在丙二醛形成的诱导阶段，α-生育酚适度下降至初始含量的约80%，而辅酶Q的总量几乎保持不变，但还原型辅酶Q9持续下降。在大量丙二醛开始形成时，辅酶Q9达到其完全氧化状态。与此同时，α-生育酚开始急剧下降，但在两个实验系统中都从未完全耗尽。显然，辅酶Q9库的氧化是线粒体中大量脂质过氧化开始以及随后α-生育酚消耗的先决条件。通过添加二硝基氯苯（谷胱甘肽转移酶的底物）捕获谷胱甘肽，导致脂质过氧化适度加速，但与对照组相比，α-生育酚和泛醇水平保持不变。向谷胱甘肽耗尽的线粒体中添加琥珀酸有效地抑制了丙二醛的形成以及α-生育酚和泛醇的消耗。数据支持这样的假设，即在缺乏线粒体谷胱甘肽的情况下，呼吸底物对脂质过氧化的保护作用是由脂溶性抗氧化剂辅酶Q和α-生育酚的再生介导的。
