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Glutatyon S-transferaz genindeki delesyonların (GSTT1 ve GSTM1) koroner arter hastalığı ve akut miyokart infarktüsü ile ilişkisi

Year 2014, Volume: 39 Issue: 2, 256 - 261, 22.07.2014
https://doi.org/10.17826/cutf.25776

Abstract

Amaç: Koroner arter hastalığı (KAH), kalp hastalıkları içerisinde en yaygın olanıdır. KAH, kalbin kendi dokusuna kan sağlayan koroner arterlerin daralması sonucunda meydana gelmektedir. Damarların daralması endotel duvarlarında kolesterol ve diğer maddelerin birikerek plak oluşumu sonucunda oluşur. Glutatyon S-Transferaz (GST) enziminin de KAH ile ilişkili olduğu bilinmektedir. GST enzimi; ksenobiyotik metabolizmasında, endojenik ve ekzojenik maddelerin detoksifikasyonunda rol oynayan önemli bir enzim grubudur. Glutatyon S-transferaz M1 (GSTM1) ve T1 (GSTT1) genleri sigara dumanında bulunan bazı kimyasalların detoksikifikasyonu veya aktivasyonu ile ilişkilidir. Bu genlerde mutasyonların olması enzimin aktivitesinin azalmasına ve KAH oluşmasına neden olur. Bu çalışmada; 1.-4. kuşaklarda KAH ve Akut Miyokart İnfarktüsü (AMİ) öyküsüne sahip bir ailede GSTM1 ve GSTT1 genleri ile ilişkisi araştırıldı. Materyal ve Metod: Bu çalışmada soy ağacı bilinen ailenin çalışmaya dahil edilen kişilerinin yaşı, sigara alkol kulanı, hastalık öyküsü kaydedildi. Probandın ortaya çıktığı kişiden başlayarak 1. ve 4. kuşakların soyağacı çıkarıldı. 1.-4. kuşaklarda yaşayan ve bulunabilen 100 kişiden venöz kan örneği alındı. GSTT1 ve GSTM1 genleri uygun primerler kullanılarak PCR yöntemi ile amplifiye edildi ve agaroz jel elektroforezinde yürütüldü. Bulgular: Bu ailede 24 kişinin KAH olduğu, bu hastaların 19 (%79)"unun da sigara kullanma alışkanlığının olduğu belirlendi. Yapılan moleküler analiz sonucunda GST polimorfizmine rastlanmadı. Sonuç: Çeşitli çalışmalarda GST geninin KAH ile ilişkili olduğu bildirilse de bizim çalışmamızda GSTT1 ve GSTM1 genlerinde polimorfizmin olmaması bu ailede ilişkili olmadığını göstermektedir. Yine sigara kullanımının GST enzim aktivitesini kesin azalttığı bildirilse de bu ailedeki koroner arter hastalığının sigara kullanımı ile de ilişkili olmadığını düşündürmektedir.

References

  • 1. Kültürsay H. Koroner Kalp Hastalığı, Primer ve Sekonder Koruma. 1.Baskı, İstanbul: ARGOS İletişim Hizmetleri Reklamcılık ve Tic. A.Ş., 2001;63-75.
  • 2. Weitzman LB. Coronary artery Disease: Heart Attack. Erişim: htpp:// www.heartcenteronline.com/myheartdr/common/articl es.cfm?ARTID=29 (Erişim Tarihi: 05.07.2008).
  • 3. Cheitlin MD, Sokolow M, Mcllroy MB. Clinical Cardiology. 6th. Ed., USA: Prentice–Hall International Inc, 1993;42-52
  • 4. Tuzcu M. Kardiovasküler Hastalıklar. Yalçın A. Cecil Essentials of Medicine. 2. Baskı, İstanbul: Yüce Yayınları A.Ş. 1991;89-115.
  • 5. Kök H. Klinik Kardiyoloji. 2.Baskı, Konya: Nobel Tıp Kitapevleri Ltd.Şti, 2002;201-14.
  • 6. Eichner JE, Dunn ST, Perveen G, et al. Apolipoprotein E Polymorphism and Cardiovascular Disease: A HuGE Review, Am J Epidemiol. 2002;155:487-95.
  • 7. Salazar LA, Hirata MH, Giannini SD, et al. Seven DNA Polymorphisms at the candidate genes of atherosclerosis in Brazilian women with angiographically document coronary artery diesease. Clinica Chemica Acta. 2000;300:139-49.
  • 8. Keterer B. Glutathione S-transferases and prevention of cellular free radical damage. Free Radical Research. 1998;28:647-58.
  • 9. Hanna E, MacLeod S, Vural E, et al. Genetic deletions of glutathione-S-transferase as a risk factor in squamous cell carcinoma of the larynx: a preliminary report. Am J Otolaryngol. 2001;22:121-3.
  • 10. Abu-Amero KK, Al-Boudari OM, Mohamed GH, et al. T null and M null genotypes of the glutathione Stransferase gene are risk factor for CAD independent of smoking. BMC Med Genet. 2006;7:1-7.
  • 11. Zhong S, Howie AF, Ketterer B, et al. Glutathione Stransferase mu locus: use of genotyping and phenotyping assays to assess association with lung cancer susceptibility. Carcinogenesis. 1991;12:1533- 7.
  • 12. Tamer L, Ercan B, Camsari A, et al. Glutathione Stransferase gene polymorphism as a susceptibility factor in smoking-related coronary artery disease. Basic Res Cardiol. 2004;99:223-9.
  • 13. Cora T, Tokac M, Acar H, et al. Glutathione Stransferase M1 and T1 genotypes and myocardial infarction. Mol Biol Rep. 2013;40:3263-7.
  • 14. Phulukdaree A, Khan S, Moodley D, et al. GST polymorphisms and early-onset coronary artery disease in young South African Indians. S Afr Med J. 2012;102:627-30.
  • 15. Taspinar M, Aydos S, Sakiragaoglu O, et al. Impact of genetic variations of the CYP1A1, GSTT1, and GSTM1 genes on the risk of coronary artery disease. DNA Cell Biol. 2012;31:211-8.
  • 16. Wilson MH, Grant PJ, Kain K, et al. Association between the risk of coronary artery disease in South Asians and a deletion polymorphism in glutathione Stransferase M1. Biomarkers. 2003;8:43-50.
  • 17. Penn A, Snyder CA. Butadiene inhalation accelerates arteriosclerotic plaque development in cockerels. Toxicology. 1996;113:351-4.
  • 18. Van Schooten FJ, Hirvonen A, Maas LM, et al. Putative susceptibility markers of coronary artery disease: association between VDR genotype, smoking, and aromatic DNA adduct levels in human right atrial tissue. Faseb J. 1998;12:1409-17.
  • 19. Girisha KM, Gilmour A, Mastana S, et al. T1 and M1 polymorphism in glutathione S-transferase gene and coronary artery disease in North Indian population. Indian J Med Sci. 2004;58:520-6.
  • 20. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Research. 1988;16:125.

Relationship between Glutathione S-transferase gene deletions (GSTT1 and GSTM1) and coronary artery disease/acute myocardial infarction.

Year 2014, Volume: 39 Issue: 2, 256 - 261, 22.07.2014
https://doi.org/10.17826/cutf.25776

Abstract

Purpose: Coronary artery disease (CAD) is the most common disease in heart-related diseases. CAD arises from the contraction of coroner artery, which provides blood for heart tissue. Glutathione S-Transferase (GST) enzymes are known to be associated with CAD. Glutathione S-Transferase M1 (GSTM1) and Glutathione S-Transferase T1 (GSTT1) genes are associated with detoxification or activation of chemicals in cigarette smoke. Mutations in these genes lead decreased enzyme activities and formation of CAD. In this study the relationship between GSTM1 and GSTT1 genes and CAD were investigated in four generations (1-4) of a family with a history of CAD and acute myocardial infarction (AMI). Material and Methods: Patients of a family with known family pedigrees included in the study. The age, use of alcohol, cigarette smoking, and disease history were recorded. Starting from the proband patient the pedigrees from first to fourth generation pedigree were examined. One-hundred venous blood samples obtained from all 4 generation individuals. Glutathione S-Transferase M1 and GSTT1 genes were amplified employing gene specific primers with PCR and visualized by agarose gel electrophoresis. Results: In this family 24 person had CAD and 19 (79%) of them were heavy cigarette smokers. As a result of the molecular analysis, we did not detect any GST polymorphisms. Conclusion: Although several lines of studies indicate an association of CAD with GST gene polymorphisms, in our study no association was found between CAD and GST polymorphisms for all family members tested. Moreover, we did not establish an association between coronary artery diseases and cigarette smoking.

References

  • 1. Kültürsay H. Koroner Kalp Hastalığı, Primer ve Sekonder Koruma. 1.Baskı, İstanbul: ARGOS İletişim Hizmetleri Reklamcılık ve Tic. A.Ş., 2001;63-75.
  • 2. Weitzman LB. Coronary artery Disease: Heart Attack. Erişim: htpp:// www.heartcenteronline.com/myheartdr/common/articl es.cfm?ARTID=29 (Erişim Tarihi: 05.07.2008).
  • 3. Cheitlin MD, Sokolow M, Mcllroy MB. Clinical Cardiology. 6th. Ed., USA: Prentice–Hall International Inc, 1993;42-52
  • 4. Tuzcu M. Kardiovasküler Hastalıklar. Yalçın A. Cecil Essentials of Medicine. 2. Baskı, İstanbul: Yüce Yayınları A.Ş. 1991;89-115.
  • 5. Kök H. Klinik Kardiyoloji. 2.Baskı, Konya: Nobel Tıp Kitapevleri Ltd.Şti, 2002;201-14.
  • 6. Eichner JE, Dunn ST, Perveen G, et al. Apolipoprotein E Polymorphism and Cardiovascular Disease: A HuGE Review, Am J Epidemiol. 2002;155:487-95.
  • 7. Salazar LA, Hirata MH, Giannini SD, et al. Seven DNA Polymorphisms at the candidate genes of atherosclerosis in Brazilian women with angiographically document coronary artery diesease. Clinica Chemica Acta. 2000;300:139-49.
  • 8. Keterer B. Glutathione S-transferases and prevention of cellular free radical damage. Free Radical Research. 1998;28:647-58.
  • 9. Hanna E, MacLeod S, Vural E, et al. Genetic deletions of glutathione-S-transferase as a risk factor in squamous cell carcinoma of the larynx: a preliminary report. Am J Otolaryngol. 2001;22:121-3.
  • 10. Abu-Amero KK, Al-Boudari OM, Mohamed GH, et al. T null and M null genotypes of the glutathione Stransferase gene are risk factor for CAD independent of smoking. BMC Med Genet. 2006;7:1-7.
  • 11. Zhong S, Howie AF, Ketterer B, et al. Glutathione Stransferase mu locus: use of genotyping and phenotyping assays to assess association with lung cancer susceptibility. Carcinogenesis. 1991;12:1533- 7.
  • 12. Tamer L, Ercan B, Camsari A, et al. Glutathione Stransferase gene polymorphism as a susceptibility factor in smoking-related coronary artery disease. Basic Res Cardiol. 2004;99:223-9.
  • 13. Cora T, Tokac M, Acar H, et al. Glutathione Stransferase M1 and T1 genotypes and myocardial infarction. Mol Biol Rep. 2013;40:3263-7.
  • 14. Phulukdaree A, Khan S, Moodley D, et al. GST polymorphisms and early-onset coronary artery disease in young South African Indians. S Afr Med J. 2012;102:627-30.
  • 15. Taspinar M, Aydos S, Sakiragaoglu O, et al. Impact of genetic variations of the CYP1A1, GSTT1, and GSTM1 genes on the risk of coronary artery disease. DNA Cell Biol. 2012;31:211-8.
  • 16. Wilson MH, Grant PJ, Kain K, et al. Association between the risk of coronary artery disease in South Asians and a deletion polymorphism in glutathione Stransferase M1. Biomarkers. 2003;8:43-50.
  • 17. Penn A, Snyder CA. Butadiene inhalation accelerates arteriosclerotic plaque development in cockerels. Toxicology. 1996;113:351-4.
  • 18. Van Schooten FJ, Hirvonen A, Maas LM, et al. Putative susceptibility markers of coronary artery disease: association between VDR genotype, smoking, and aromatic DNA adduct levels in human right atrial tissue. Faseb J. 1998;12:1409-17.
  • 19. Girisha KM, Gilmour A, Mastana S, et al. T1 and M1 polymorphism in glutathione S-transferase gene and coronary artery disease in North Indian population. Indian J Med Sci. 2004;58:520-6.
  • 20. Miller SA, Dykes DD, Polesky HF. A simple salting out procedure for extracting DNA from human nucleated cells. Nucleic Acids Research. 1988;16:125.
There are 20 citations in total.

Details

Primary Language Turkish
Journal Section Research
Authors

Semra Koç This is me

Davut Alptekin This is me

Publication Date July 22, 2014
Published in Issue Year 2014 Volume: 39 Issue: 2

Cite

MLA Koç, Semra and Davut Alptekin. “Glutatyon S-Transferaz Genindeki delesyonların (GSTT1 Ve GSTM1) Koroner Arter hastalığı Ve Akut Miyokart infarktüsü Ile ilişkisi”. Cukurova Medical Journal, vol. 39, no. 2, 2014, pp. 256-61, doi:10.17826/cutf.25776.