Jung Marianna E, Agarwal Rajnee, Simpkins James W
Department of Pharmacology and Neuroscience, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA.
Neurosci Lett. 2007 Apr 12;416(2):160-4. doi: 10.1016/j.neulet.2007.01.065. Epub 2007 Feb 2.
Cytochrome c oxidase (COX) is a key mitochondrial enzyme that catalyzes electron transfer at the terminal stage of respiratory chain and is composed of multisubunits. We hypothesize that ethanol withdrawal (EW) impairs the activity of COX and estrogen deprivation exacerbates this problem. Five-month-old ovariectomized rats with or without 17beta-estradiol (E2) replacement received a control dextrin or a liquid ethanol diet (6.5%, 5 weeks). They were then sacrificed either during ethanol exposure or at 24h of EW (EW group). Mitochondria of the cerebellum and cortex were processed to measure the activities of total COX, COX subunit I, and IV. The effects of EW and E2 on the protein levels of these subunits were also assessed using an immunoblotting method. As compared to the control dextrin and ethanol exposure, EW decreased the activities of total COX, COX I, and COX IV. E2 treatment prevented the effects of EW on the activities of total COX and COX IV but not COX I. Neither EW nor E2 altered the protein levels of the subunits. These findings suggest that a counteracting relationship exists between the effects of EW and E2 on the activity of COX in a subunit specific manner.
细胞色素c氧化酶（COX）是一种关键的线粒体酶，它在呼吸链的末端阶段催化电子传递，由多个亚基组成。我们假设乙醇戒断（EW）会损害COX的活性，而雌激素缺乏会加剧这一问题。五个月大的去卵巢大鼠，分为接受或未接受17β-雌二醇（E2）替代治疗两组，分别给予对照糊精或液体乙醇饮食（6.5%，5周）。然后在乙醇暴露期间或EW 24小时时（EW组）将它们处死。对小脑和皮质的线粒体进行处理，以测量总COX、COX亚基I和IV的活性。还使用免疫印迹法评估了EW和E2对这些亚基蛋白质水平的影响。与对照糊精和乙醇暴露相比，EW降低了总COX、COX I和COX IV的活性。E2治疗可防止EW对总COX和COX IV活性的影响，但对COX I无效。EW和E2均未改变亚基的蛋白质水平。这些发现表明，EW和E2对COX活性的影响之间存在一种亚基特异性的拮抗关系。
