http://www.cnr.it/ontology/cnr/individuo/prodotto/ID109027

GSTM1, GSTT1 and CYP1A1 detoxification gene polymorphisms and susceptibility to smoking-related coronary artery disease (Abstract/Poster in convegno)

Type

Abstract/Poster in convegno (Classe)
Prodotto della ricerca (Classe)

Label

GSTM1, GSTT1 and CYP1A1 detoxification gene polymorphisms and susceptibility to smoking-related coronary artery disease (Abstract/Poster in convegno) (literal)

Anno

2006-01-01T00:00:00+01:00 (literal)

Alternative label

Manfredi S.; Botto N.; Rizza A.; Federici C.; Andreassi M. G. (2006)
GSTM1, GSTT1 and CYP1A1 detoxification gene polymorphisms and susceptibility to smoking-related coronary artery disease
in European Heart Journal
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Manfredi S.; Botto N.; Rizza A.; Federici C.; Andreassi M. G. (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

European Heart Journal, 27 -. Abstract Supplement. European Society of Cardiology, 2006. (literal)

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Background: Cigarette smoking is a powerful risk factor for atherosclerosis, but the degree of damage varies from individual to individual. Genetic polymorphisms of relevant xenobiotic metabolising enzymes may determine the susceptibility of an individual response to environmental toxicants. Aim: To assess whether the inheritance of polymorphic genes encoding cytochrome P450 1A1 (CYP1A1) and glutathione S transferase (GSTM1 and GSTT1) have an effect in modulating smoking-related coronary artery disease (CAD) risk. Methods: CYP1A1 (6235TC) polymorphism and the GSTM1, GSTT1 null genotypes were evaluated by PCR-restriction fragment length polymorphism (RFLP) in a group of 164 smoker patients (143 male, 57.8±10.3 years) consecutively referred to our Department for coronary angiography investigation. Significant CAD was 50% diameter reduction in at least 1 major coronary vessel. Results: Significant CAD was detected in 115 patients (70.1%). Gender (p0.0001), diabetes 2 (pC polymorphism (p=0.13) were not significantly different between patients with or without CAD. The frequency of the GSTT1 null genotype was 42.6% in the CAD patients compared with 24.5% in the no-CAD group (p=0.03). After adjustment for traditional risk factors, the presence of GSTT1 null genotype was significantly associated with an increased risk of CAD (OR=2.6; 95% CI: 1-6.8, p=0.04). Moreover, smokers with the null GSTT1 genotype had a significant increased risk for three-vessel disease than those with the positive genotype (?2=15.5, p=0.002). Conclusion: Smokers carrying null GST genotype have an increased susceptibility to the smoking related CAD. (literal)

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