Abstract
Oxidative stress, the accumulation of oxygen free radicals (reactive oxygen species) above and beyond the capacity of a cell to utilise antioxidant systems to detoxify these potentially damaging molecules, is a common feature of many human disorders. Cigarette smoke is not only a source of free radicals but is also a potent stimulator of the intracellular production of free radicals, by the mitochondrial electron transport chain and the plasmalemmal NADPH oxidase. Adding to this free radical burden is the reduction, by cigarette smoke, of the cellular antioxidant capacity. Together, the increased production and reduced detoxification of free radicals has been strongly linked to smoking-induced diseases including atherosclerotic cardiovascular disease, cancer and chronic obstructive pulmonary disease (COPD). In this review, we discuss the mechanisms underlying cellular free radical production, relate this to the three major smoking-related human diseases listed above and present potential mechanisms by which cigarette smoke may increase the oxidative burden on cells and contribute to disease.
Keywords: reactive oxygen species, antioxidants, cardiovascular disease, atherosclerosis, cancer, chronic obstructive pulmonary disease, COPD, cigarette smoke, Oxidative stress, NADPH oxidase
Mini-Reviews in Organic Chemistry
Title: The Role of Oxidative Stress in Smoking-Related Diseases
Volume: 8 Issue: 4
Author(s): Ian M. Fearon, Gary Phillips, Tony Carr, Mark Taylor, Damien Breheny and Stephen P. Faux
Affiliation:
Keywords: reactive oxygen species, antioxidants, cardiovascular disease, atherosclerosis, cancer, chronic obstructive pulmonary disease, COPD, cigarette smoke, Oxidative stress, NADPH oxidase
Abstract: Oxidative stress, the accumulation of oxygen free radicals (reactive oxygen species) above and beyond the capacity of a cell to utilise antioxidant systems to detoxify these potentially damaging molecules, is a common feature of many human disorders. Cigarette smoke is not only a source of free radicals but is also a potent stimulator of the intracellular production of free radicals, by the mitochondrial electron transport chain and the plasmalemmal NADPH oxidase. Adding to this free radical burden is the reduction, by cigarette smoke, of the cellular antioxidant capacity. Together, the increased production and reduced detoxification of free radicals has been strongly linked to smoking-induced diseases including atherosclerotic cardiovascular disease, cancer and chronic obstructive pulmonary disease (COPD). In this review, we discuss the mechanisms underlying cellular free radical production, relate this to the three major smoking-related human diseases listed above and present potential mechanisms by which cigarette smoke may increase the oxidative burden on cells and contribute to disease.
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Cite this article as:
M. Fearon Ian, Phillips Gary, Carr Tony, Taylor Mark, Breheny Damien and P. Faux Stephen, The Role of Oxidative Stress in Smoking-Related Diseases, Mini-Reviews in Organic Chemistry 2011; 8 (4) . https://dx.doi.org/10.2174/157019311797440317
DOI https://dx.doi.org/10.2174/157019311797440317 |
Print ISSN 1570-193X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6298 |
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