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.
journal_name
Int J Environ Res Public Healthauthors
Rendu F,Peoc'h K,Berlin I,Thomas D,Launay JMdoi
10.3390/ijerph8010136subject
Has Abstractpub_date
2011-01-01 00:00:00pages
136-47issue
1eissn
1661-7827issn
1660-4601pii
ijerph8010136journal_volume
8pub_type
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pub_type: 杂志文章,meta分析,评审
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