Monoamine oxidases and tobacco smoking (original) (raw)

Journal Article

Department of Pharmacology, Pitié-Salpêtrière University Hospital, Paris

Address for correspondence: Dr I. Berlin, Department of Pharmacology, Pitié-Salpêtrière University Hospital, 47 bd de l'Hôpital, 75013 Paris, France. Tel.: 33 1 42 16 16 78_Fax_:

33 1 42 16 16 88

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Robert M. Anthenelli

Department of Psychiatry, University of Cincinnati, College of Medicine and Veterans Affairs Medical Center, Cincinnati, Ohio, USA

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Revision received:

10 October 2000

Accepted:

29 October 2000

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Abstract

Although nicotine has been identified as the main ingredient in tobacco responsible for aspects of the tobacco dependence syndrome, not all of the psychopharmacological effects of smoking can be explained by nicotine alone. Accumulating preclinical and clinical evidence has demonstrated that smoking also leads to potent inhibition of both types (A and B) of monoamine oxidase (MAO). Smokers have 30–40 % lower MAOB and 20–30 % lower MAOA activity than non-smokers. Reduced MAO activity in smokers has been shown by direct measures (platelets, positron emission tomographic studies) or by indirect measures (concentration of monoamine catabolites in plasma or CSF). We examine the hypothesis that chronic habitual smoking can be better understood in the context of two pharmacological factors: nicotine and reduced MAO activity. We speculate that MAO inhibition by compounds found in either tobacco or tobacco smoke can potentiate nicotine's effects. Based on this concept, more effective anti-smoking drug strategies may be developed. As a practical consequence of tobacco smoke's MAO-inhibitory properties, comparative psychiatric research studies need to screen and control for tobacco use.

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