Branca D, Roberti M S, Lorenzin P, Vincenti E, Scutari G
Department of Biological Chemistry, University of Padova, Italy.
Biochem Pharmacol. 1991 Jun 21;42(1):87-90. doi: 10.1016/0006-2952(91)90684-w.
Isolated rat liver mitochondria have been incubated in the presence of the general anesthetic 2,6-diisopropylphenol (0-100 microM) and the efficiency of oxidative phosphorylation has been evaluated by measuring the respiratory rates, the rates of ATP synthesis or hydrolysis and the magnitude of the transmembrane electrical potential. The results obtained indicate that: (a) in mitochondria energized either by succinate or by ATP, 2,6-diisopropylphenol decreased the transmembrane electrical potential and increased the rates of either electron transfer or ATP hydrolysis; (b) in succinate-energized mitochondria 2,6-diisopropylphenol, at concentrations causing substantial depression of the transmembrane electrical potential, did not modify either the rate of phosphorylation of added ADP or the rate of ADP-stimulated respiration: (c) in succinate-energized mitochondria 2,6-diisopropylphenol caused a concentration-dependent inhibition of the uncoupler-stimulated rate of succinate oxidation. These findings suggest that under the experimental conditions reported 2,6-diisopropylphenol affected the generation and/or maintenance of the transmembrane electrical potential while leaving unchanged the coupling between the electron flow in the respiratory chain and the synthesis of ATP.
将分离出的大鼠肝脏线粒体置于全身麻醉剂2,6 - 二异丙基苯酚（0 - 100微摩尔）存在的环境中进行孵育，并通过测量呼吸速率、ATP合成或水解速率以及跨膜电势大小来评估氧化磷酸化效率。所得结果表明：（a）在由琥珀酸或ATP供能的线粒体中，2,6 - 二异丙基苯酚降低了跨膜电势，并提高了电子传递或ATP水解的速率；（b）在由琥珀酸供能的线粒体中，2,6 - 二异丙基苯酚在导致跨膜电势显著降低的浓度下，既未改变添加ADP的磷酸化速率，也未改变ADP刺激的呼吸速率；（c）在由琥珀酸供能的线粒体中，2,6 - 二异丙基苯酚对解偶联剂刺激的琥珀酸氧化速率产生浓度依赖性抑制作用。这些发现表明，在所报道的实验条件下，2,6 - 二异丙基苯酚影响了跨膜电势的产生和/或维持，而呼吸链中电子流动与ATP合成之间的偶联未发生改变。
