The lack of association between monoamine oxidase (MAO) intron 13 polymorphism and platelet MAO-B activity among men

Pivac, Nela and Knežević, Jelena and Mustapić, Maja and Deželjin, Martina and Muck-Šeler, Dorotea and Kozarić-Kovačić, Dragica and Balija, Melita and Matijević, Tanja and Pavelić, Jasminka (2006) The lack of association between monoamine oxidase (MAO) intron 13 polymorphism and platelet MAO-B activity among men. Life Sciences, 79 (1). pp. 45-49. ISSN 0024-3205

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Abstract

Monoamine oxidase (MAO), a mitochondrial flavine containing enzyme, exists in two isoenzymes, MAO-A and MAO-B. Platelets contain MAO-B subtype, proposed to be a biomarker for different personality characteristics and vulnerability for substance abuse. The most common polymorphism of MAO-B gene, a single base change (A or G) occurs in intron 13. It has been proposed to be a functional polymorphism, controlling the activity of MAO-B in platelets. The aim of the study was to determine the association between platelet MAO-B activity and MAO-B intron 13 polymorphism in 225 racially and ethnically uniform healthy Caucasian men of the Croatian origin. Our results showed that platelet MAO-B activity did not differ between subjects subdivided into those with A-allele or G-allele. This polymorphism of the MAO-B gene did not control the activity of the MAO-B in platelets. Platelet MAO-B activity was associated only with the smoking status, and it was significantly decreased in smokers when compared to nonsmokers. No significant association was found between MAO-B polymorphism and smoking status. In healthy individuals of the Croatian origin, the studied MAO-B polymorphism showed a lack of functional importance in regulating MAO-B activity in platelets. Since different populations may vary in the association between functional polymorphism and the MAO-B activity, and the genotype of transcription factor AP-2β was reported to be associated with altered platelet MAO-B activity, and with specific personality traits, further studies on different populations should be conducted to elucidate the molecular mechanism/s regulating platelet MAO-B activity.

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