TY - CHAP M1 - Book, Section TI - Redox Signaling and Oxidative Stress in Lung Diseases A1 - Deshane, Jessy A1 - Thannickal, Victor J. A2 - Grippi, Michael A. A2 - Elias, Jack A. A2 - Fishman, Jay A. A2 - Kotloff, Robert M. A2 - Pack, Allan I. A2 - Senior, Robert M. A2 - Siegel, Mark D. PY - 2015 T2 - Fishman's Pulmonary Diseases and Disorders, 5e AB - Molecular oxygen is a prerequisite to life of all aerobic organisms. The human lung with its large surface area and extensive blood supply is engineered for its primary function in gas exchange. While oxygen is essential for its many roles in human physiology, high concentrations of oxygen or its metabolites, commonly referred to as reactive oxygen species (ROS), have the potential to cause cellular injury and contribute to disease pathogenesis. The most damaging forms of ROS are free radicals. A free radical, by definition, refers to any chemical species containing one or more unpaired electrons in their atomic or molecular orbitals. These unpaired electron(s) give considerable reactivity to free radical species, which can trigger chemical reactions that damage cellular constituents of living organisms. Molecular oxygen (dioxygen) is itself, a radical based on the presence of unpaired electrons in its outermost orbital; however, their parallel spin retrains its reactivity. O2 can form the superoxide anion radical (O2•−) upon addition of an electron; thus, overcoming this restraint and making O2•− a highly reactive species.1,2 The photodynamic activation of oxygen can result in the formation of singlet oxygen, and its reductive activation results in the formation of hydrogen peroxide (H2O2) or the highly reactive hydroxyl radical (•OH).3,4 When two free radicals share their unpaired electrons, nonradical species of lower reactivity are generated. Thus, ROS constitute both free radicals and nonradicals. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/11/03 UR - accessmedicine.mhmedical.com/content.aspx?aid=1122356394 ER -