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Interaction between CYP1A1 T3801C and AHR G1661A polymorphisms according to smoking status on blood pressure in the Stanislas cohort

Gambier, Nicolasa; Marteau, Jean-Bricea; Batt, Anne-Mariea; Marie, Bérangèrea; Thompson, Annickb; Siest, Gérarda; Foernzler, Dorotheeb; Visvikis-Siest, Sophiea

doi: 10.1097/01.hjh.0000249697.26983.aa
Original papers: Genetic aspects
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Background CYP1A1, one of the key enzymes in detoxifying toxic components produced during cigarette smoking, is regulated by aromatic hydrocarbon receptor (AHR). A CYP1A1 T3801C polymorphism, associated with a higher CYP1A1 inducibility and enhanced catalytic activity, has been linked to stroke, triple vessel disease and may, therefore, be associated with blood pressure (BP). The relation of the widely studied G1661A polymorphism of the human AHR gene with BP is unknown.

Objectives To investigate the genetic influence of CYP1A1 T3801C and AHR G1661A polymorphisms on BP in relation to tobacco consumption.

Design and participants Study participants were selected from a French longitudinal cohort of volunteers for a free health check-up. These individuals (302 men and 311 women) were not taking medication that can affect blood pressure. Information about active smoking status was obtained by a self-administered questionnaire.

Results After multiple regression analysis, systolic blood pressure (SBP) and diastolic blood pressure (DBP) did not differ significantly according to their tobacco status excepted for DBP in men. In addition, neither CYP1A1 T3801C nor AHR G1661A polymorphism was linked to blood pressure. However, systolic and diastolic blood pressures differed significantly according to CYP1A1 T3801C genotype between ex-smokers and smokers. Finally, the interaction between CYP1A1 T3801C and AHR G1661A polymorphisms explained a significant difference of SBP and DBP between carriers of both CYP1A1-C3801 and AHR-A1661 alleles.

Conclusion This study is the first to show an interaction between the CYP1A1 T3801C and AHR G1661A polymorphisms. This interaction could explain the difference in blood pressure level between smokers and non-smokers/ex-smokers but needs to be confirmed in a large sample.

aINSERM U525, Faculté de Pharmacie, Université Henri Poincaré Nancy 1, Nancy, France

bRoche Center for Medical Genomics, F. Hoffmann-La Roche, Ltd PRG, Basel, Switzerland

Received 9 January, 2006

Revised 1 June, 2006

Accepted 12 June, 2006

Correspondence and requests for reprints to Dr Sophie Visvikis-Siest, INSERM U525, Equipe 4, Faculté de Pharmacie, 30, Rue Lionnois, 54000 Nancy, France Tel: +33 3 83 68 21 58; fax: +33 3 83 32 13 22; e-mail: Sophie.Visvikis-Siest@nancy.inserm.fr

Sponsorship: This work was supported by an INSERM Grant: IDS (Interactions entre les déterminants de la santé). The Stanislas cohort study is supported by the Caisse Nationale d'Assurance Maladies des Travailleurs Salariés (CNAM), The Institut National de la Santé et de la Recherche Médicale (INSERM), the Région Lorraine, the Communauté Urbaine du Grand Nancy and by Roche Molecular Systems (Alameda, USA).

© 2006 Lippincott Williams & Wilkins, Inc.