Smoking Related Diseases: The Central Role of Monoamine Oxidase

Francine Rendu, Katell Peoc’h, Ivan Berlin, Daniel Thomas and Jean-Marie Launay
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Francine Rendu: UMRS 956 (Génétique, Pharmacologie et Physiopathologie des maladies cardiovasculaires), Faculté de Médecine Pitié-Salpétrière, Université Pierre et Marie Curie, 91 Bd de l’hôpital, 75634 Paris cedex 13, France
Katell Peoc’h: Service de Biochimie et Biologie Moléculaire, Assistance Publique des Hôpitaux de Paris (AP-HP), and Biologie cellulaire, Faculté de Pharmacie, Université Paris-Descartes, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris cedex 10, France
Ivan Berlin: Pharmacologie clinique du tabagisme, Inserm U894, Faculté de Médecine Pitié-Salpétrière, Université Pierre et Marie Curie and Service de pharmacologie, Hôpital Pitié-Salpétrière, 47 Bd de l'Hôpital, 75651 Paris cedex13, France
Daniel Thomas: Institut de Cardiologie, Hôpital Pitié-Salpétrière, 47 Bd de l'Hôpital, 75651 Paris cedex13, France
Jean-Marie Launay: Service de Biochimie et Biologie Moléculaire, Assistance Publique des Hôpitaux de Paris (AP-HP), and Biologie cellulaire, Faculté de Pharmacie, Université Paris-Descartes, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris cedex 10, France

IJERPH, 2011, vol. 8, issue 1, 1-12

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.

Keywords: smoking; serotonin; norepinephrine; monoamine oxidase; cardiovascular; platelets; epigenetic; cancer; depression (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2011
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