作者: Ganesh V. Sangle , Subir K. Roy Chowdhury , Xueping Xie , Gerald L. Stelmack , Andrew J. Halayko
DOI: 10.1016/J.FREERADBIOMED.2009.12.017
关键词:
摘要: Abstract Coronary artery disease (CAD) is the leading cause of mortality in diabetic patients. Mitochondrial dysfunction and increased production reactive oxygen species (ROS) are associated with diabetes CAD. Elevated levels glycated LDL (glyLDL) were detected patients diabetes. Our previous studies demonstrated that glyLDL generation ROS altered activities antioxidant enzymes vascular endothelial cells (EC). This study examined effects on consumption mitochondria key mitochondrial electron transport chain (ETC) cultured porcine aortic EC. The results treatment significantly impaired Complexes I, II/III, IV ETC EC compared to or vehicle control using oxygraphy. Incubation reduced membrane potential, NAD + /NADH ratio, (NADH-ubiquinone dehydrogenase, succinate cytochrome c reductase, ubiquinone oxidase) control. abundance mitochondria-associated release from after treatment. findings suggest attenuates ETC, decreases consumption, reduces increases EC, which potentially contribute