title: Oxidative stress in obstructive sleep apnea and intermittent hypoxia--revisited--the bad ugly and good: implications to the heart and brain.
abstract: Obstructive sleep apnea (OSA), characterized by intermittent hypoxia (IH), is linked with increased reactive oxygen species/reactive nitrogen species (ROS/RNS) and oxidative stress, which adversely affect the associated cardio-/cerebro-vascular disease in OSA. Yet, animal and a small number of human studies support activation of cardio-/cerebro-protective mechanisms as well. ROS/RNS are intricate and multifaceted molecules with multiple functions. At low-moderate concentrations ROS/RNS are considered "good", by regulating vital cellular functions. At higher levels, they are considered "bad" by promoting oxidative stress and damaging vital macromolecules through ischemia and reperfusion (I/R) injury. Subsequently, ROS/RNS can get "ugly" by eliciting sterile inflammation and a multitude of deadly pathologies. What makes ROS/RNS good, bad, or ugly? A dynamic interplay between a large number of factors determines the outcomes. These include the types of ROS/RNS produced, their quantity, duration, frequency, intracellular localization, micro-environmental antioxidants, as well as the genetic make-up and life style related variables. This review presents the currently available data on redox biology in physiological/pathophysiological conditions and in OSA/IH, in order to better understand the apparently contradictory findings on damage vs. repair. These findings are discussed within the context of the prevailing views on I/R associated ROS/RNS, and their potential implications to OSA.
authors.affiliation: The Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, POB 9649, 31096 Haifa, Israel. Electronic address: lenal@tx.technion.ac.il.
authors.forename: Lena
authors.initials: L
authors.lastname: Lavie
mesh_terms: D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000503:physiopathology*
chemical_list: D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species
keywords: Acute myocardial infarction; Anti-oxidants; Coronary collaterals; Endothelial progenitor cells; Ischemia/reperfusion; Ischemic preconditioning; Obstructive sleep apnea; Oxidative stress; ROS/RNS; Stroke