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Vol 48(2014) N 6 p. 823-834; DOI 10.1134/S0026893314060090 Full Text

G.F. Korytina1*, L.Z. Akhmadishina1, O.V. Kochetova1, Yu.V. Burduk2, Yu.G. Aznabaeva2, Sh.Z. Zagidullin2, T.V. Victorova1,2

Association of genes involved in nicotine and tobacco smoke toxicant metabolism (CHRNA3/5, CYP2A6, and NQO1) and DNA repair (XRCC1, XRCC3, XPC, and XPA) with chronic obstructive pulmonary disease

1Institute of Biochemistry and Genetics, Ufa Research Center, Russian Academy of Sciences, Ufa, 450054 Russia
2Bashkortostan State Medical University, Ufa, 45000 Russia

*guly_kory@mail.ru
Received - 2014-04-29; Accepted - 2014-06-27

Polymorphisms of the CHRNA5/A3, CYP2A6, NQO1, XPC, XRCC1, CRCC3, XPD, and XPA genes were tested for association with the development and progression of chronic obstructive pulmonary disease (COPD) in ethnic Tatars. CHRNA5 (rs16969968) (P = 0.0001, OR = 2.24) and CHRNA3 (rs1051730) (P = 0.0001, OR = 2.72) polymorphisms were associated with COPD development in the recessive model. The non-deletion variant of CYP2A6 (del) was associated with COPD risk (P = 0.00001, OR = 2.77). NQO1 (rs113341), XRCC1 (rs25487), XRCC3 (rs86539), XPC (rs2228001), and XPA (rs1800975) were associated with COPD in the additive model (P = 0.000001, OR = 2.67; P = 0.00001, OR = 0.51; P = 0.0003, OR = 1.76; P = 0.0004, OR = 0.54; and P = 0.007, OR = 0.74, respectively). A gene-by-environment interaction was observed for XPA (rs1800975) and the smoking status (Pinteract = 0.002), and the rs16969968 and rs1051730 polymorphisms of the CHRNA3/5 gene cluster showed an association with COPD only in smokers. Carriers of the CYP2A6 deletion (CYP2A6*4) had a lower smoking index (P = 0.0019). XRCC3 (rs861539) genotype TT was characterized by lower indices of pulmonary function, including vital capacity (VC) (P = 0.0487), forced vital capacity (FVC) (P = 0.0032), and forced expiratory volume in 1 second (FEV1) (P = 0.02). FVC was found to depend on the genotype at XPA (rs1800975) (P = 0.0028).

chronic obstructive pulmonary disease, association, gene-by-environment interaction, nicotine dependence, oxidative stress, DNA repair



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