The role of oxidative stress in the biological responses of lung epithelial cells to cigarette smoke

Abstract

The mechanism(s) by which cigarette smoke contributes to lung diseases, such as cancer, remains unclear. Recent developments in our knowledge of cell signalling events suggest that cigarette smoke causes oxidative stress and proinflammatory responses in cells of the lung. Cigarette smoke is a complex mixture of over 4000 compounds and high levels of oxidants and reactive oxygen species (ROS) have been detected in both mainstream and sidestream smoke. Oxidative stress that ensues, when the antioxidant defences are depleted, is accompanied by increases in ROS production in lung epithelial cells. Cigarette smoke-mediated oxidative stress produces DNA damage and activates survival signalling cascades resulting in uncontrolled cell proliferation and transformation. Intervention studies using antioxidants have provided compelling evidence that oxidative stress plays a critical role in the aetiology of smoking-related disorders.

NF-κB and STAT3 signaling pathways collaboratively link inflammation to cancer

“…During tumor initiation, an infl ammatory microenvironment can enhance the proliferation of mutated cells (Hussain and Harris, 2007;Polyak et al, 2009;Wang et al, 2010). In addition, inflammatory cells can also increase mutation rates through serving as sources of reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI) that are able to induce DNA damage and genomic instability (Miletic et al, 2007;Faux et al, 2009;Pan et al, 2009;Hursting and Berger, 2010;Zargan et al, 2011). The process of tumor growth from a single initiating cell into a fully developed primary tumor is called tumor promotion, which is stimulated by infl ammation-driven mechanism.…”

Effects of Different Phases of Cigarette Smoke on Lipid Peroxidation and Membrane Structure in Liposomes

“…[63] Several studies suggest that the LPO products may be considered as pertinent biomarkers of harm. [15,[64][65][66][67] The essential part of their conclusions is based on the experimental data acquired in vivo and through using cell culture probes. [64][65][66][67][68] There exists very limited experimental material available through in vitro studies.…”

“…[2] Thus, cigarette smoking, which is considered in the literature as a risk factor for various pathological developments and diseases (such as chronic bronchitis, emphysema, cardiovascular disease, carcinogenic developments, and tumour growth [7][8][9][10][11][12][13][14] ) causes, in particular, the oxidative damage of cell membranes and biological macromolecules. [6,[15][16][17][18][19][20][21][22][23] Cigarette smoke is a complex chemical conglomerate that contains high concentrations of two distinctly different fractions of free radicals, one in its gas phase (GP) and another one in the particulate matter (tar). [16,17,[24][25][26][27] The GP of the smoke predominantly contains reactive carbon-and oxygencentred radicals, as well as a rather sizable amount of nitric oxide.…”

Comparative cytoprotective effects of carbocysteine and fluticasone propionate in cigarette smoke extract-stimulated bronchial epithelial cells

“…The sources of the increased oxidative stress in COPD patients derive from the increased burden of inhaled oxidants such as cigarette smoke and from the increase in ROS generated by several inflammatory, immune and structural airways cells (Faux et al 2009). We tested the effect of CSE on ROS production in bronchial epithelial cells at three different time points (2, 4 and 18 h) to test whether a short-or a long-term incubation was suitable for evaluating ROS formation.…”