Grant C M, MacIver F H, Dawes I W
C.R.C. for Food Industry Innovation, School of Biochemistry and Molecular Genetics, University of New South Wales, Sydney, Australia.
FEBS Lett. 1997 Jun 30;410(2-3):219-22. doi: 10.1016/s0014-5793(97)00592-9.
Yeast strains that lack mitochondrial function are sensitive to oxidative stress caused by reactive oxygen species (ROS). Specifically, rho0 mutants that lack mitochondrial DNA, and strains deleted for the nuclear genes COX6 and COQ3 that are required for function of the respiratory electron transport chain, were sensitive to H2O2. In addition, treatment with mitochondrial inhibitors including antimycin A, oligomycin, potassium cyanide and sodium azide increased sensitivity to H2O2. The mechanism does not appear to depend on the antioxidant status of the cell since respiratory-deficient strains were able to mount an inducible adaptive response to H2O2. We suggest that the oxidant sensitivity is due to a defect in an energy-requiring process that is needed for detoxification of ROS or for the repair of oxidatively damaged molecules.
缺乏线粒体功能的酵母菌株对活性氧(ROS)引起的氧化应激敏感。具体而言,缺乏线粒体DNA的rho0突变体,以及缺失呼吸电子传递链功能所需的核基因COX6和COQ3的菌株,对过氧化氢敏感。此外,用包括抗霉素A、寡霉素、氰化钾和叠氮化钠在内的线粒体抑制剂处理会增加对过氧化氢的敏感性。该机制似乎不依赖于细胞的抗氧化状态,因为呼吸缺陷型菌株能够对过氧化氢产生诱导性适应性反应。我们认为,氧化敏感性是由于ROS解毒或氧化损伤分子修复所需的能量需求过程存在缺陷。