Cigarette Smoke-Induced Oxidative Stress in Type I and Type II Lung Epithelial Cells
Cigarette smoke (CS) is a complex combination of over 5000 compounds divided into two phases (tar and gas) whose exposure causes various lung pathological conditions especially COPD and cancer. In a single puff, tar phase basically contains extremely high concentrations of stable and long-lived radicals (~1017 radicals/gm), whereas gas phase contains ~1015 organic radicals. In contrast to stable life radicals (e.g., hydrogen peroxide, hypochlorous acid) present in tar phase, the radicals in gaseous phase are highly reactive nitrogen and oxygen-centered radicals (e.g., nitric oxide, reactive olefins, dienes) known to have lifetime of less than 1 s. Therefore, cigarette smoke constituents evoke the endogenous oxidants production and agitate normal functioning of tissues, especially type I and II pulmonary epithelium. As a result of smoke exposure, increased level of oxidants (exogenous or endogenous) leads to stress state termed as “oxidative stress,” which arises due to commotion in prooxidant and antioxidant balance in favor of the prooxidant. The oxidative stress caused by the constituents of cigarette smoke in normal as well as in the mutated cells leads to activation of various upstream signaling events such as activation of lipid-specific enzymes especially phospholipases whose role is crucial in the regulation and remodeling of membrane lipids when subjected to hazardous and noxious environmental insults such as cigarette smoke-initiated tissue damage.
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