Trümper L, Schönfeld P, Augustin W
Institut für Biochemie, Medizinische Akademie Magdeburg, DDR.
Biomed Biochim Acta. 1989;48(2-3):S44-7.
In the early phase of iron/ascorbate induced peroxidation in rat liver mitochondria a progressively diminished active and uncoupled respiration, likely caused by an attack at the level of the respiratory chain was established, whereas the transmembrane potential (delta psi) under phosphorylating conditions did, however, not reflect this inhibition. A tentative explanation for this behaviour was suggested on the basis of an impairment of both membrane potential generating and consuming processes. By measurements of the velocity of mitochondrial 32Pi-uptake during the time course of peroxidation an inhibition of the Pi-carrier was detected. The calculated flux control coefficients for the Pi- and ATP/ADP-translocator indicate that the last one exerts a large control independent on the respiration rate during the initial phase of peroxidation. The data show that the predominant step in the control of oxidative phosphorylation at the site of the consumers must be attributed to the ATP/ADP-exchanger.
在铁/抗坏血酸诱导大鼠肝线粒体过氧化的早期阶段，已证实活性呼吸和非偶联呼吸逐渐减弱，这可能是由于呼吸链水平受到攻击所致，而磷酸化条件下的跨膜电位（δψ）却并未反映出这种抑制作用。基于膜电位产生和消耗过程均受损这一情况，提出了对该现象的初步解释。通过测量过氧化过程中线粒体32Pi摄取的速度，检测到Pi载体受到抑制。计算得出的Pi和ATP/ADP转运体的通量控制系数表明，在过氧化初始阶段，后者发挥着与呼吸速率无关的较大控制作用。数据显示，在消耗位点对氧化磷酸化进行控制的主要步骤必须归因于ATP/ADP交换体。
