RT Book, Section A1 Deshane, Jessy A1 Thannickal, Victor J. A2 Grippi, Michael A. A2 Antin-Ozerkis, Danielle E. A2 Dela Cruz, Charles S. A2 Kotloff, Robert M. A2 Kotton, Camille Nelson A2 Pack, Allan I. SR Print(0) ID 1194947558 T1 Redox Signaling and Oxidative Stress in Lung Diseases T2 Fishman’s Pulmonary Diseases and Disorders, 6e YR 2023 FD 2023 PB McGraw-Hill Education PP New York, NY SN 9781260473988 LK accessmedicine.mhmedical.com/content.aspx?aid=1194947558 RD 2025/03/18 AB Molecular oxygen is a prerequisite to life of all aerobic organisms. With its large surface area and extensive blood supply the human lung 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 electrons 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.