The Intercontinental Journal of Internal Medicine aims to publish issues related to all fields of internal medicine of the highest scientific and clinical value at an international level and accepts articles on these topics.

EndNote Style
Original Article
Evaluation of antioxidant activity in without persistent ST-segment elevation
Aims: Coronary artery disease is the most common cause of mortality and morbidity worldwide. Oxidative stress is involved in the pathogenesis of many diseases, including atherosclerosis. Thiols are important antioxidants for the elimination of reactive oxygen radicals and oxidative stress. In this study, we aimed to compare patients suffering from without persistent ST-segment elevation (NSTMI) and volunteers with normal coronary arteries in terms of antioxidants.
Methods: The study included 105 patients diagnosed with NSTMI and 51 controls. Plasma total thiol, native thiol, and disulfide levels were measured.
Results: Baseline demographic characteristics were similar between the groups. The ejection fraction was lower in the patient group. In terms of biochemical and hematologic parameters, glucose, AST, ALT, white blood cell count, and troponin were higher in the patient group, while other parameters were similar. Plasma native thiol (344.32 ± 81.28 µmol/L versus 403.62 ± 62.36 µmol/L, p < 0.0001) and total thiol (382.90 ± 91.13 µmol/L versus 444.17 ± 65.53 µmol/L, p < 0. 0001) levels were lower in NSTMI patients compared to control patients, while disulfide (19.29± 3.19 versus 20.27± 8.10, p = 0.77) levels were similar between the groups.
Conclusion: In this study, we found that native thiol and total thiol levels, which are antioxidant markers, were lower in patients with NSTMI compared with the control group. Our study shows that antioxidant activity is affected in NSTMI, and antioxidant levels are decreased.

1. Menees DS, Bates ER. Evaluation of patients with suspected coronaryartery disease. Coron Artery Dis. 2010;21(7):386-390.
2. Badimon L and Vilahur G. Thrombosis formation on atheroscleroticlesions and plaque rupture. J Intern Med. 2014;276(6):618-632.
3. Vogiatzi G, Tousoulis D, Stefanadis C: The role of oxidative stress inatherosclerosis. Hellenic J Cardiol. 2009;50 (5):402-409.
4. Bonomini F, Tengattini S, Fabiano A, Bianchi R, Rezzani R:Atherosclerosis and oxidative stress. Histol Histopathol. 2008;23(3):381-390.
5. Stocker R, Keaney JF: Role of oxidative modifications in atherosclerosis.Physiol Rev. 2004;84(4):1381-1478.
6. Leopold JA, Loscalzo J. Oxidative risk for atherothromboticcardiovascular disease. Free Rad Biol Med. 2009;47(12):1673-1706.
7. Lubos E, Loscalzo J, Handy D. Glutathione peroxidase-1 in health anddisease: From molecular mechanisms to therapeutic opportunities.Antiox Red Sig. 2011;15(7):1957-1997.
8. Kundi H, Gok M, Kiziltunc E, Cetin M, Ornek E. Association of IGF-1 with coronary collateral circulation in stable coronary artery disease.Biomark Med. 2017;11(7):527-534.
9. Leopold JA. Antioxidants and coronary artery disease: frompathophysiology to preventive therapy. Coron Artery Dis.2015;26(2):176-183.
10. Altıparmak IH, Erkuş ME, Sezen H, et al. The relation of serum thiollevels and thiol/disulphide homeostasis with the severity of coronaryartery disease. Kardiol Pol. 2016;74(11):1346-1353.
11. Kiziltunc E, Gok M, Kundi H, et al. Plasma thiols and thiol-disulfidehomeostasis in patients with isolated coronary artery ectasia.Atherosclerosis. 2016;253:209-213.
12. Cremers CM, Jakob U. Oxidant sensing by reversible disulfide bondformation. J Biol Chem. 2013;288(37):26489-26496.
13. Collet JP, Thiele H, Barbato E, et al.: ESC Scientific Document Group.2020 ESC Guidelines for the management of acute coronary syndromesin patients presenting without persistent ST-segment elevation. EurHeart J. 2021;42(14):1289-1367.
14. Erel O, Neselioglu S. A novel and automated assay for thiol/disulphidehomeostasis. Clin Biochem. 2014;47(18):326-332.
15. Nickening G, Harrison DG. The AT-1-type angiotensin receptorin oxidative stress and hypertension part I: oxidative stress andatherogenesis. Circulation. 2002;105(3):393-396.
16. Ray R, Shah AM. NADPH oxidase and endothelial cell function. ClinSci. 2005; 109(3):217-226
17. Griendling KK, FitzGerald GA. Oxidative stress and cardiovascularinjury part 1: basic mechanisms and in vivo monitoring of ROS.Circulation. 2003;108(16):1912-1916.
18. Sies H. Total antioxidant capacity: appraisal of a concept. J Nutr.2007;137(6):1493-1495.
19. Wang Y, Chun OK, Song WO. Plasma and dietary antioxidant statusas cardiovascular disease risk factors: a reviewof human studies.Nutrients. 2013;5(8):2969-3004.
20. Vaziri ND. Causal link between oxidative stress, inflammation, andhypertension. Iran J Kidney Dis. 2008;2(1):1-10.
21. Cai H, Harrison DG. Endothelial dysfunction in cardiovasculardiseases: the role of oxidant stress. Circ Res. 2000;87(10):840-844.
22. Majzunova M, Dovinova I, Barancik M, Chan JYH. Redox signaling inpathophysiology of hypertension. J Biomed Sci. 2013;20(1):69.
23. Ng C-Y, Yusof K, Othman F, Jaarin K. The role of repeatedly heatedsoybean oil in the development of hypertension in rats: association withvascular inflammation. Int J Exp Pathol. 2012;93(5):377-387.
24. Steyers III CM, Miller Jr JF. Endothelial dysfunction in chronicinflammatory diseases. Int J Mol Sci. 2014;15(7):1324-1349.
25. Agan V, Celik H, Eren MA,et al. Investigation of oxidative stress andthiol/disulphide homeostasis in Graves&rsquo; disease. Medicina (Kaunas).2019;55(6):275.
26. Biswas S, Chida AS, Rahman I. Redox modifications of protein-thiols:emerging roles in cell signaling. Biochem Pharmacol. 2006;71(5):551-564.
27. Koken,T. Kahraman, A. Serteser, M. Hemodiyalizin protein karbonili&ccedil;erigi ve s&uuml;lfidril grupları &uuml;zerine etkisi. T&uuml;rk Nefrol Diyal TransplantDerg. 2001;10(2):64-66.
28. Sen, C.K. Packer, L. Thiol homeostasis and supplements in physicalexercise. Am J Clin Nutr. 2000;72(2):653-669.
29. Elcik D, Kelesoglu S, Yilmaz Y, et al. Relationship between thiol,disulphide volume and contrast-induced nephropathy in acute coronarysyndrome patients treated with percutaneous coronary intervention.Scand J Clin Lab Invest. 2021;81(3):173-180
Volume 1, Issue 3, 2023
Page : 59-62