Oxidative Damage and Chronic Inflammation Induced by Smoking: Potential Antioxidant and Peripheral Biomarker Considerations

Abstract

Several studies indicate that oxidative stress and inflammation are features of smoking related disorders. Active smoking can cause respiratory disorders culminating in chronic obstructive pulmonary disease (COPD), cardiovascular hazards, and cancer. Lung cancer results from man-made and natural environmental exposures acting in concert with both genetic and acquired characteristics. Genetic polymorphisms that affect xenobiotic metabolism or cellular response to DNA damage can modulate individual sensitivity to genotoxins. Endogenous antioxidant defences are often inadequate to scavenge free radicals (contained in cigarette smoke), reactive oxygen (ROS) and reactive nitrogen species (RNS) completely and ongoing oxidative damage to DNA, lipids, proteins, and other biomolecules is suggested to contribute to the pathology of many human degenerative diseases. The phenolic compounds in plant extracts are mostly derivatives, and/or isomers of flavones, isoflavones, flavonols, catechins, tocopherols, and phenolic acids. These are accessible to consumers through diet, their multifunctional nature (in particular flavonoids) makes them ideal candidates as prophylactic agents. There is a need to define if the presence of oxidative stress induced by smoking could be attenuated by the administration of antioxidant compounds and if this relationship could be linked to the presence of a particular genetic polymorphism and modulation of the complex cell signalling cascades involving gene transcription. (Cancer Prevention Res 10, 149- 158, 2005)