Impact of Glutathione S-Transferase M1 and T1 Gene Polymorphisms on the Smoking-Related Coronary Artery Disease.
10.3346/jkms.2008.23.3.365
- Author:
Soo Joong KIM
1
;
Myeong Gon KIM
;
Kwon Sam KIM
;
Jung Sang SONG
;
Sung Vin YIM
;
Joo Ho CHUNG
Author Information
1. Department of Cardiology, Internal Medicine, Kyunghee University College of Medicine, Seoul, Korea. soojoong@dreamwiz.com
- Publication Type:Original Article
- Keywords:
Glutathione Transferase;
Polymorphism, Genetic;
Smoking;
Coronary Artery Disease
- MeSH:
Aged;
Coronary Angiography;
Coronary Artery Disease/epidemiology/*genetics/radiography;
Female;
Genetic Predisposition to Disease/epidemiology;
Genotype;
Glutathione Transferase/*genetics;
Humans;
Male;
Middle Aged;
*Polymorphism, Genetic;
Risk Factors;
Severity of Illness Index;
Smoking/epidemiology/*genetics
- From:Journal of Korean Medical Science
2008;23(3):365-372
- CountryRepublic of Korea
- Language:English
-
Abstract:
Glutathione S-transferase (GST) plays a key role in the detoxification of xenobiotic atherogen generated by smoking. To analyze the effect of GSTM1/T1 gene polymorphisms on the development of smoking-related coronary artery disease (CAD), 775 Korean patients who underwent coronary angiography were enrolled. The subjects were classified by luminal diameter stenosis into group A (>50%), B (20-50%), or C (<20%). GSTM1 and GSTT1 gene polymorphisms were analyzed using multiplex polymerase chain reaction (PCR) for GSTM1/T1 genes and CYP1A1 gene for internal control. Of 775 subjects, 403 patients belonged to group A. They had higher risk factors for CAD than group B (N=260) and group C (N=112). The genotype frequencies of null GSTM1 and GSTT1 showed no significant differences among 3 groups. Considering the effect of GSTM1 gene polymorphisms on the smoking-related CAD, smokers with GSTM1 null genotype had more increased risk for CAD than non-smoker with GSTM1 positive genotype (odds ratios [OR], 2.07, confidence interval [CI], 1.06-4.07). Also the effect of GSTT1 gene polymorphism on smoking-related CAD showed the same tendency as GSTM1 gene (OR, 2.00, CI, 1.05-3.84). This effect of GSTM1/T1 null genotype on smoking-related CAD was augmented when both gene polymorphisms were considered simultaneously (OR, 2.76, CI, 1.17-6.52). We concluded that GSTM1/T1 null genotype contributed to the pathogenesis of smoking-related CAD to some degree.
