Abstract
Smoking is a major risk factor of morbidity and mortality. It is well established that monoamine oxidase (MAO) activity is decreased in smokers. Serotonin (5-HT), a major substrate for MAO that circulates as a reserve pool stored in platelets, is a marker of platelet activation. We recently reported that smoking durably modifies the platelet 5-HT/MAO system by inducing a demethylation of the MAO gene promoter resulting in high MAO protein concentration persisting more than ten years after quitting smoking. The present data enlarges the results to another MAO substrate, norepinephrine (NE), further confirming the central role of MAO in tobacco use-induced diseases. Thus, MAO could be a readily accessible and helpful marker in the risk evaluation of smoking-related diseases, from cardiovascular and pulmonary diseases to depression, anxiety and cancer. The present review implements the new finding of epigenetic regulation of MAO and suggests that smoking-induced MAO demethylation can be considered as a hallmark of smoking-related cancers similarly to other aberrant DNA methylations.
Highlights
Pharmacologie clinique du tabagisme; Inserm U894, Facultéde Médecine Pitié-Salpétrière, UniversitéPierre et Marie Curie and Service de pharmacologie, Hôpital Pitié-Salpétrière, Institut de Cardiologie, Hôpital Pitié-Salpétrière, 47 Bd de l'Hôpital, 75651 Paris cedex13, France; Tel.: +33-(0)140-779-907; Fax: +33-(0)140-779-645
For those for which monoamine oxidase (MAO) amount was over the median value, considered as a cut off value, it significantly correlated with the length of smoking: the longest time they smoked, the higher amount of MAO they had
This review summarizes our recent finding that smoking durably reduces the methylation of the MAOB promoter, leading to an increase in MAO-B protein synthesis
Summary
Tobacco use is the leading cause of preventable death and morbidity worldwide. Smoking is a modifiable risk factor for three major diseases, namely cardiovascular diseases, pulmonary diseases and cancer. Among cardiovascular risks factors, smoking is second following dyslipidemia, with no threshold, no incidence of the length of smoking and a major prevalence among people less than 50 years for both sexes [1] It is a major determinant of chronic obstructive pulmonary disease (COPD) and the most important risk factor of lung cancer. While nicotine is considered to be the major player underlying tobacco dependence [2], many other tobacco smoke constituents are involved in smoking-induced dependence and diseases, including additives to enhance the addictiveness [3,4,5]. MAO have been shown to be impacted by smoking [6,7,8]
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