Estimating a smoker's health may utilise approaches based on the role of oxidative stress in pathogenic developments. In this context, oxidative stress is often considered as an imbalance in redox processes. Nevertheless, our analysis of the literature showed that although this imbalance may indeed furnish the chief cause of oxidative stress, it does not always provide sufficient condition on redox processes themselves. Cigarette smoke is a source of reactive oxygen species (ROS), which may cause oxidative modifications of biomolecules and intervene as signalling agents in adaptational and regulatory mechanisms. The protracted exposure of the smoker to smoke-borne and secondary (cell-derived) ROS is considered as one of the reasons for aging and weakening of the cellular antioxidant defense systems. However, to date little account has been taken of the fact that cigarette smoke is also a supplier of inhibitory species that retard free-radical processes, and whose role in triggering oxidative stress has barely been studied. Based on literature data (> 5000 publications), we have carried out a comprehensive analysis of potential biomarkers and regulators of oxidative stress. We conclude that at the current stage of knowledge it is untimely to consider smoking as the necessary immediate prerequisite of oxidative stress. Instead, we believe that to proceed from redox imbalance to oxidative stress, and in doing so triggering cellular dysfunctions, one should consider the coupling regulatory entity. The latter may be considered as the phase of accumulation of disturbances in the functioning of biological structures.