101. Smoking related diseases: the central role of monoamine oxidase.
- Author
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Rendu F, Peoc'h K, Berlin I, Thomas D, and Launay JM
- Subjects
- Anxiety enzymology, Anxiety epidemiology, Biomarkers metabolism, Cardiovascular Diseases enzymology, Cardiovascular Diseases epidemiology, Depression enzymology, Depression epidemiology, Humans, Hydroxyindoleacetic Acid metabolism, Lung Diseases enzymology, Lung Diseases epidemiology, Methoxyhydroxyphenylglycol analogs & derivatives, Methoxyhydroxyphenylglycol metabolism, Neoplasms enzymology, Neoplasms epidemiology, Norepinephrine metabolism, Risk Factors, Serotonin metabolism, Smoking physiopathology, Epigenesis, Genetic, Monoamine Oxidase genetics, Monoamine Oxidase metabolism, Smoking metabolism
- 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.
- Published
- 2011
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