Gene-Smoking Interaction on Ischemic Stroke: Case-Control Study of Glutathione S-Transferase Polymorphism
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Background: Smoking is a major risk factor of stroke, but not all smokers develop stroke. This individual difference could be explained by the variation of detoxification capacity. We investigated the relationship of smoking with the genetic polymorphism of a detoxification enzyme (glutathione S-transferase: GST). Methods: This study was conducted as a case-control study. Conventional risk factors for stroke and 3 genetic polymorphisms of GST (GSTM1, GSTT1 , and GSTP1 ) were studied in both 290 acute ischemic stroke patients and 290 age and sex matched controls. Smoking status was determined by urinary cotinine level. The effect of interaction of GST polymorphisms and smoking on stroke risk was investigated. Results: Stroke patients had higher cotinine level compared to that of control (P <0.01). There was little difference between the patient group and control group with regard to the GST polymorphism alone, but significant interaction was noticed between the GST polymorphism and the smoking status. When we stratified the group according to the smoking status by cotinine level, stroke was significantly more frequent in GSTM1 null type and GSTT1, GSTP1 wild type of the high cotinine level group (OR and 95% CI: 2.115,1.219-3.670; 2.620, 1.480-4.638; 2.212, 1.343-3.644 respectively). Conclusion: GST polymorphisms interact with the smoking and confer an increased risk of ischemic stroke, indicating that genetic polymorphism of GST might reveal smokers who are more susceptible to the ischemic stroke.
Abstract
Background: Smoking is a major risk factor of stroke, but not all smokers develop stroke. This individual difference could be explained by the variation of detoxification capacity. We investigated the relationship of smoking with the genetic polymorphism of a detoxification enzyme (glutathione S-transferase: GST). Methods: This study was conducted as a case-control study. Conventional risk factors for stroke and 3 genetic polymorphisms of GST (GSTM1, GSTT1 , and GSTP1 ) were studied in both 290 acute ischemic stroke patients and 290 age and sex matched controls. Smoking status was determined by urinary cotinine level. The effect of interaction of GST polymorphisms and smoking on stroke risk was investigated. Results: Stroke patients had higher cotinine level compared to that of control (P <0.01). There was little difference between the patient group and control group with regard to the GST polymorphism alone, but significant interaction was noticed between the GST polymorphism and the smoking status. When we stratified the group according to the smoking status by cotinine level, stroke was significantly more frequent in GSTM1 null type and GSTT1, GSTP1 wild type of the high cotinine level group (OR and 95% CI: 2.115,1.219-3.670; 2.620, 1.480-4.638; 2.212, 1.343-3.644 respectively). Conclusion: GST polymorphisms interact with the smoking and confer an increased risk of ischemic stroke, indicating that genetic polymorphism of GST might reveal smokers who are more susceptible to the ischemic stroke.
참고문헌 (19)
- Wolf PA, "Cigarette smoking as a risk factor for stroke. The framingham study", JAMA, 259, pp.1025~1029 (1988)
- Shinton R, "Meta-analysis of relation between cigarette smoking and stroke", BMJ, 298, pp.789~794 (1989)
- Ambrose JA, "The pathophysiology of cigarette smoking and cardiovascular disease: An update", J Am Coll Cardiol, 43, pp.1731~1737 (2004)
- Stocker R, "New insights on oxidative stress in the artery wall", J Thromb Haemost, 3, pp.1825~1834 (2005)
- Dusinska M, "Glutathione s-transferase polymorphisms influence the level of oxidative DNA damage and antioxidant protection in humans", Mutat Res, 482, pp.47~55 (2001)
- Strange RC, "Glutathione s-transferase: Genetics and role in toxicology", Toxicol Lett, 112, pp.357~363 (2000)
- Townsend DM, "The importance of glutathione in human disease", Biomed Pharmacother, 57, pp.145~155 (2003)
- Tamer L, "Glutathione s-transferase gene polymorphism as a susceptibility factor in smoking-related coronary artery disease", Basic Res Cardiol, 99, pp.223~229 (2004)
- Wilson MH, "Glutathione s-transferase m1 null genotype is associated with a decreased risk of myocardial infarction", FASEB J, 14, pp.791~796 (2000)
- Girisha KM, "T1 and m1 polymorphism in glutathione s-transferase gene and coronary artery disease in north indian population", Indian J Med Sci, 58, pp.520~526 (2004)
- Um JY, "Glutathione s-transferase gene polymorphism and ischemic cerebrovascular disease", Int J Neurosci, 116, pp.55~65 (2006)
- Turkanoglu A, "Association analysis of GSTT1., GSTM1 genotype polymorphisms and serum total GST activity with ischemic stroke risk", Neurol Sci, 31, pp.727~734 (2010)
- Parker DR, "The accuracy of self-reported smoking status assessed by cotinine test strips", Nicotine Tob Res, 4, pp.305~309 (2002)
- Ryberg D, "Genotypes of glutathione transferase m1 and p1 and their significance for lung DNA adduct levels and cancer risk", Carcinogenesis, 18, pp.1285~1289 (1997)
- Morita S, "Association between genetic polymorphisms of glutathione s-transferase p1 and n-acetyltransferase 2 and susceptibility to squamous-cell carcinoma of the esophagus", Int J Cancer, 79, pp.517~520 (1998)
- Gore JM, "Validity of serum total cholesterol level obtained within 24 hours of acute myocardial infarction", Am J Cardiol, 54, pp.722~725 (1984)
- Yan B, "When to measure lipid profile after stroke?", Cerebrovasc Dis, 19, pp.234~238 (2005)
- Sillett RW, "Deception among smokers", Br Med J, 2, pp.1185~1186 (1978)
- Apseloff G, "The importance of measuring cotinine levels to identify smokers in clinical trials", Clin Pharmacol Ther, 56, pp.460~462 (1994)