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Reactive oxygen species (ROS) in cardioprotection: which ROS does the signaling?
Anders O. Garlid¹, Matthew Gold¹, Martin Jaburek², and Keith D. Garlid¹
¹Portland State University, Dept. of Biology Portland OR, USA (aogarlid@gmail.com)
²Dept. of Membrane Transport Biophysics, Institute of Physiology, Prague, Czech Republic
ROS are the second messengers of cardioprotective signaling; however, the ROS species responsible for this effect under physiological conditions is not known. Cellular ROS transformations proceed from superoxide (O₂-) to hydrogen peroxide (H₂O₂) and then to hydroxyl radical (•OH), each of which has been investigated as the signaling ROS. H₂O₂ is an appealing candidate for a second messenger because it is relatively stable and can readily diffuse to target kinases. Nevertheless, there is no direct evidence to support or exclude H₂O₂ as the physiological ROS messenger. We examined the effects of exogenous H₂O₂ and endogenous (mitochondrial) ROS produced by the electron transport chain on three ROS-dependent processes: PKCε-dependent mitochondrial ATP-sensitive potassium channel (mitoKATP) opening, PKCε-dependent inhibition of the mitochondrial permeability transition (MPT), and cardioprotection of the ex vivo heart. Dimethylsulfoxide (DMSO) and dimethylformamide (DMF) scavenge •OH but neither influenced PKCε activation by exogenous H₂O₂. This indicates that they neither scavenge H₂O₂ nor are they thiol reductants. However, both reagents blocked PKCe activation by endogenous (mitochondrial) ROS, and DMF blocked cardioprotection by diazoxide and ischemic postconditioning. The putative •OH scavenger N-2-mercaptopropionylglycine (MPG) blocked PKCε activation by exogenous H₂O₂, indicating that MPG is acting here as a thiol reductant rather than as a ROS scavenger. These results appear to exclude H₂O₂ as the signaling ROS and implicate a downstream oxidation product of •OH. Our evidence points to hydroperoxy fatty acids as the signaling ROS in cardioprotection.
Keywords: mitochondria; cardioprotection; hydroxyl radical; K-ATP channels; cardiac ischemia; hydroperoxy fatty acids; ROS signaling