Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review

Abstract

Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species (ROS) is widely accepted as a primary molecular event that predisposes individuals to these smoking-related ailments. This review focused on how cigarette smoke (CS) promotes ROS formation rather than the pathophysiological repercussions of ROS and oxidative stress. A comprehensive analysis of existing studies revealed the following key ways through which CS imposes ROS burden on biological systems: (1) ROS, as well as radicals, are intrinsically present in CS, (2) CS constituents generate ROS through chemical reactions with biomolecules, (3) CS stimulates cellular ROS sources to enhance production, and (4) CS disrupts the antioxidant system, aggravating the ROS generation and its functions. While the evidence supporting these mechanisms is chiefly based on in vitro and animal studies, the direct clinical relevance remains to be fully elucidated. Nevertheless, this understanding is fundamental for deciphering molecular events leading to oxidative stress and for developing intervention strategies to counter CS-induced oxidative stress.

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

“…Cigarette smoke contains high concentrations of ROS-generating substances like superoxide radicals, nitric oxide, and peroxynitrite. Inhalation of cigarette smoke has been shown to quickly deplete circulating antioxidant reserves in smokers as well (Seo et al 2023). Carcinogens in cigarette smoke also drive the formation of reactive DNA aldehydes like formaldehyde that can interfere with DNA repair pathways.…”

Endocrine-disrupting compounds and their impact on human placental function: evidence from placenta organ-on-chip studies

“…Trophoblasts are sensitive to oxidative stress, as reflected by ex vivo studies that demonstrate decreased proliferation upon nicotine exposure but with potential concomitant upregulation of antioxidant enzymes. 126,127 This is in contrast with other 2D-culture systems from other culture systems. For instance, in pulmonary endothelial cells, and in rat brain apoptotic populations were observed to increase upon CSE exposure.…”

Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases

“… 64 Of these, active or passive smoking may lead to an excessive intake or improper utilization of iron as cigarette smoke (CS) contains high levels of ROS. 65 The ensuing cellular oxidative stress then triggers inflammation, cellular senescence and death. Initial research has indicated that exposure to CS induces the buildup of iron and ferritin in cells that line the lungs and in immune cells within the air sacs, while increasing levels of ferritin and non-heme iron in the bloodstream.…”