Mezera Vojtech, Endlicher Rene, Kucera Otto, Sobotka Ondrej, Drahota Zdenek, Cervinkova Zuzana
Department of Physiology, Faculty of Medicine in Hradec Kralove, Charles University in Prague, 500 38 Hradec Kralove, Czech Republic; Buck Institute for Research on Aging, Novato, CA 94945, USA.
Department of Anatomy, Faculty of Medicine in Hradec Kralove, Charles University in Prague, 500 38 Hradec Kralove, Czech Republic.
Oxid Med Cell Longev. 2016;2016:7573131. doi: 10.1155/2016/7573131. Epub 2016 Dec 15.
Epigallocatechin gallate (EGCG) is a green tea antioxidant with adverse effects on rat liver mitochondria and hepatocytes at high doses. Here, we assessed whether low doses of EGCG would protect these systems from damage induced by tert-butyl hydroperoxide (tBHP). Rat liver mitochondria or permeabilized rat hepatocytes were pretreated with EGCG and then exposed to tBHP. Oxygen consumption, mitochondrial membrane potential (MMP), and mitochondrial retention capacity for calcium were measured. First, 50 M EGCG or 0.25 mM tBHP alone increased State 4 Complex I-driven respiration, thus demonstrating uncoupling effects; tBHP also inhibited State 3 ADP-stimulated respiration. Then, the coexposure to 0.25 mM tBHP and 50 M EGCG induced a trend of further decline in the respiratory control ratio beyond that observed upon tBHP exposure alone. EGCG had no effect on MMP and no effect, in concentrations up to 50 M, on mitochondrial calcium retention capacity. tBHP led to a decline in both MMP and mitochondrial retention capacity for calcium; these effects were not changed by pretreatment with EGCG. In addition, EGCG dose-dependently enhanced hydrogen peroxide formation in a cell- and mitochondria-free medium. . Moderate nontoxic doses of EGCG were not able to protect rat liver mitochondria and hepatocytes from tBHP-induced mitochondrial dysfunction.
表没食子儿茶素没食子酸酯（EGCG）是一种绿茶抗氧化剂，高剂量时对大鼠肝脏线粒体和肝细胞有不良影响。在此，我们评估了低剂量的EGCG是否能保护这些系统免受叔丁基过氧化氢（tBHP）诱导的损伤。用EGCG预处理大鼠肝脏线粒体或通透化的大鼠肝细胞，然后使其暴露于tBHP。测量了氧气消耗、线粒体膜电位（MMP）和线粒体钙保留能力。首先，单独使用50μM EGCG或0.25 mM tBHP可增加状态4复合体I驱动的呼吸作用，从而显示出解偶联效应；tBHP还抑制状态3 ADP刺激的呼吸作用。然后，同时暴露于0.25 mM tBHP和50μM EGCG会导致呼吸控制率进一步下降，且下降趋势超过单独暴露于tBHP时观察到的情况。EGCG对MMP没有影响，在浓度高达50μM时，对线粒体钙保留能力也没有影响。tBHP导致MMP和线粒体钙保留能力均下降；EGCG预处理并未改变这些效应。此外，EGCG在无细胞和线粒体的培养基中剂量依赖性地增强了过氧化氢的形成。中等无毒剂量的EGCG无法保护大鼠肝脏线粒体和肝细胞免受tBHP诱导的线粒体功能障碍。
