An Insight into Cellular and Molecular Changes Associated with Cigarette Smoking: A Review

Cigarette is a mixture of chemicals in which the major component is nicotine. Nicotine results in addiction and its effects are initiated by damaging lipids, activating oxidative sensitive pathways, DNA and other components of the cell. Long-term use of cigarettes causes both stimulatory and inhibitory responses of various cells involved in the secretion of chemokines and cytokines which are known inflammatory markers. In the smoke, particulate phases of cigarettes and smoke consumption causes oxidative/nitrosative stress leads to various diseases. Previous findings from cigarette smoke intake show stimulatory effect by increasing cytokines inside the immune cells and also suppression of immune cells by decreasing the production of cytokines from T-cells which was due to oxidative stress by a generation of ROS and RNS, leads to chronic inflammation. This review provides recent findings from cigarette smoke exposure in experimental animals, mainly smoke-associated free radical-mediated lipids auto-oxidation, nitric oxide-mediated cerebral blood flow, regulation of heme oxygenase, neurokinin (NKR-1) receptors, metalloproteinases (MMPs), and Toll-like receptors (TLRs). These were found to be few targets in the antigen-presenting cells that are involved in invading foreign micro-organisms which are affected by cigarette smoke and they can be a potential target for therapeutic interventions in lung cancer and other tobacco-associated diseases.