MnSOD, CAT and GPx-3 genetic polymorphisms in coronary artery disease
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In this study, we aimed to determine the gene polymorphisms of antioxidant enzymes that determine or affect antioxidant activity in the occurrence of the disease and/or complications during and after the surgery in patients who were decided to undergo coronary artery bypass surgery due to coronary artery disease. Blood samples taken before operation in 26 coronary artery patients who were decided to be operated according to the international procedure and the phenol/chloroform method was used to isolate DNA. DNA samples were amplified by using polymerase chain reaction (PCR) method with specific primers for MnSOD, CAT, GPx-3 antioxidant gene regions. As a result of the increasing process, the PCR products for the purpose of determining gene polymorphism, NGOMIV SMA f and BSA I restriction enzymes were used for MNSOD, CAT and GPx-3 gene region, respectively. Allele frequencies were determined and compared by Chi square test. VV (46.15%) and VA (53.85%) genotype for MnSOD region, i TT (22.22%), TC (16.67%) and CC (61.11%) genotype for CAT region, and CC (12.50%), TC (25%) and TT (62.50%) genotypes for GPx-3 region were obtained. While there was no statistically significant significance in terms of genotypes obtained in MnSOD and GPx-3 gene regions (P > 0.05), a significant difference was found in the CAT gene region in terms of genotypes (P < 0.01). Although oxidative stress is important in relation to cardiovascular diseases and postoperative complications, virtually no study of antioxidant enzymes in gene polymorphism are included in the literature. Work is lacking in relation to the subject.
KeywordsMnSOD GPx-3 CAT Polymorphism Coronary artery
This study was funded by Cumhuriyet Üniversitesi (Grant no 1) and Bitlis Eren Üniversitesi (Grant no 2).
- 1.Grundy SM, Pasternak R, Greenland P, Smith S Jr, Fuster V (1999) Assesment of cardiovascular risk by use of multiple risk factor assessment equation. A statement for healthcare professionals from the American Heart Association and the American College of cardiology. Circulation 100:1481–1492CrossRefGoogle Scholar
- 11.Shukla V, Mishra SK, Pant HC (2011) Oxidative stress in neurodegeneration. Adv Pharmacol Scl 572–634Google Scholar
- 12.Paravicini TM, Touyz RM (2006) Redox signaling in hypertension. Cardiovasc Res 247–258Google Scholar
- 15.Pearson TA, Mensah GA, Alexander RW et al (2003) Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the centers for disease control and prevention ant the American Heart Association. Circulation 107(3):499–511CrossRefGoogle Scholar
- 16.Doğan A, Türker FS (2017) Cardiopulmonary bypass and oxidative stress. Chem Res J 2(6):156–162Google Scholar
- 21.Sambrook J, Fritsch EF, Maniatis T (1989) Molecular cloning: A laboratory manual. 2nd ed. Cold Spring Harbor Laboratory Pres, Cold Spring Harbor. pp 9.16–9.19Google Scholar
- 22.Forsberg L, Lyrenas L, Faire UD, Morgenstern R (2001) A common functional C–T substitution polymorphism in the promoter region of the human catalase gene influences transcription factor binding, reporter gene transcription and is correlated to blood catalase levels. Free Radical Biol Med 30(5):500–505CrossRefGoogle Scholar
- 23.Voetsch B, Jin RC, Bierl C, Benke KS, Kenet G, Simioni P, Ottaviano F, Damasceno BP, Annichino-Bizacchi JM, Handy DE, Loscalzo J (2007) Promoter polymorphisms in the plasma glutathione peroxidase (GPx-3) gene: a novel risk factor for arterial ischemic stroke among young adults and children. Stroke 38(1):41–49CrossRefGoogle Scholar
- 27.Neomoto M, Nishimura R, Sasaki T, Hiki Y, Miyashita Y, Nishioka M, Fujimoto K, Sakuma T, Ohashi T, Fukuda K, Eto Y, Tajima N (2007) Genetic association of glutathione peroxidase-1 with coronary artery calcification in type 2 diabetes: a case control study with multi-slice computed tomography. Cardiovasc Diabetol 6:23–27CrossRefGoogle Scholar