作者: Stephen J. Ralph , Rafael Moreno-Sánchez , Jiri Neuzil , Sara Rodríguez-Enríquez
DOI: 10.1007/S11095-011-0566-7
关键词: Cancer cell 、 Dehydrogenase 、 NAD+ kinase 、 Citric acid cycle 、 Biology 、 Reactive oxygen species 、 Biochemistry 、 Oxidative phosphorylation 、 Oxidative stress 、 Mitochondrion
摘要: Succinate:quinone reductase (SQR) of Complex II, occupying a unique central point in the mitochondrial respiratory system as major source electrons driving reactive oxygen species (ROS) production, is an ideal pharmaceutical target for modulating ROS levels normal cells to prevent oxidative stress-induced damage or increase cancer cells, inducing cell death. Value drugs like diazoxide protecting while vit. E analogues promote kill them, highlighted. As pharmaceuticals, agents may degenerative disease; their modes action are being fully explored. Evidence that SDH/Complex II tightly coupled NADH/NAD+ ratio all impacted by available supplies Krebs cycle intermediates essential NAD-linked substrates, and NAD+-dependent regulation reviewed, links dehydrogenases, I E3 dihiydrolipoamide dehydrogenase produce ROS. We collate discuss diverse sources information relating production different biological systems, focussing on evidence SQR main mitochondria, particularly its relevance protection from stress mitochondrial-targeted anticancer (mitocans) novel therapies.