Tobacco smoke constituents affecting oxidative stress

Abstract

Cigarette smoke has considerable potential for inducing oxidative modifications and depletion of antioxidants. In cigarette smoke-exposed aqueous solutions, ROS and RNS form and subsequently act as potent oxidants. Oxidative damage to lipids, proteins, and DNA by cigarette smoke-derived ROS and RNS has been extensively demonstrated both in vitro and in vivo. In many cases, the initially generated reactive intermediates convert cellular constituents into second-generation reactive intermediates (e.g., acrolein, 4-hydroxynonenal) capable of inducing further cytotoxic and genotoxic damage. When free radicals react with nonradicals (e.g., lipids), new radicals can form that may result in a chain reaction of free radicals. Thus, relatively short-lived free radicals may propagate their damaging effects beyond the limits set by their short half-lives and limited diffusion times. ROS and RNS activate numerous redox sensitive signaling pathways that modulate cellular responses, such as inflammation, which may itself result in the formation of endogenous oxidative species. Therefore, the oxidative damage resultant from cigarette smoke exposure is complex and likely mediated by both the oxidative potential of cigarette smoke and indirect biological responses. © Springer-Verlag Berlin Heidelberg 2006.