Oxidant and antioxidant status in coronary artery disease

Bastani,Abdolhossein; Rajabi,Sadegh; Daliran,Afshin; Saadat,Habibollah; Karimi-Busheri,Feridoun

doi:10.3892/br.2018.1130

Oxidant and antioxidant status in coronary artery disease

Authors:
- Abdolhossein Bastani
- Sadegh Rajabi
- Afshin Daliran
- Habibollah Saadat
- Feridoun Karimi-Busheri
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Affiliations: Department of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran 1985717443, Iran, Cardiovascular Research Center, Modares Hospital, Shahid Beheshti University of Medical Sciences, Tehran 1998734383, Iran, Department of Oncology, University of Alberta, Edmonton, AB T6G 1Z2, Canada
Published online on: July 17, 2018 https://doi.org/10.3892/br.2018.1130
Pages: 327-332

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Abstract

Formation of atherosclerotic plaques is the major cause of coronary artery disease (CAD). Several lines of study have revealed the role of oxidative stress in CAD pathogenesis. In the present study the aim was to investigate the oxidative and antioxidative markers in CAD patients and a control population. The study sample comprised of acute coronary syndrome (ACS) patients, chronic CAD patients and healthy controls (n=30/group). Blood samples of patients and control subjects were collected to measure the concentrations of reduced glutathione (GSH), malondialdehyde (MDA) and the percentage of MDA release as well as the activity of erythrocyte glutathione peroxidase (GPx) and total antioxidant capacity (TAC) of plasma. All parameters were measured by spectrophotometric methods. Additionally, oxidant/antioxidant status was compared between CAD patients with single, double or triple-vessel stenosis and in comparison with controls. The results indicated a significant increase in MDA level and the percentage of MDA release (P<0.05), and a marked decrease in GSH concentration (P<0.0001), TAC (P<0.0001) and the activity of erythrocyte GPx (P<0.0001) in the patient groups compared controls. ACS patients exhibited a similar pattern of data when compared with the chronic CAD group. Similar results were also observed when chronic CAD patients with single, double or triple vessel stenosis and controls were compared. The present study indicates that the acute form of CAD is more susceptible to oxidative damage, suggesting that use of antioxidant therapy may be warranted to ameliorate oxidative stress in this condition.

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1	Pathak LA, Shirodkar S, Ruparelia R and Rajebahadur J: Coronary artery disease in women. Indian Heart J. 69:532–538. 2017. View Article : Google Scholar : PubMed/NCBI
2	Wong ND: Epidemiological studies of CHD and the evolution of preventive cardiology. Nat Rev Cardiol. 11:276–289. 2014. View Article : Google Scholar : PubMed/NCBI
3	Hansson GK: Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 352:1685–1695. 2005. View Article : Google Scholar : PubMed/NCBI
4	Badimon L and Vilahur G: Thrombosis formation on atherosclerotic lesions and plaque rupture. J Intern Med. 276:618–632. 2014. View Article : Google Scholar : PubMed/NCBI
5	Zaman AG, Helft G, Worthley SG and Badimon JJ: The role of plaque rupture and thrombosis in coronary artery disease. Atherosclerosis. 149:251–266. 2000. View Article : Google Scholar : PubMed/NCBI
6	Wick G and Grundtman C: Inflammation and Atherosclerosis. I. Springer-Verlag Wien; Austria: 2011
7	Cervantes Gracia K, Llanas-Cornejo D and Husi H: CVD and oxidative stress. J Clin Med. 6:222017. View Article : Google Scholar
8	Vogiatzi G, Tousoulis D and Stefanadis C: The role of oxidative stress in atherosclerosis. Hellenic J Cardiol. 50:402–409. 2009.PubMed/NCBI
9	Bonomini F, Tengattini S, Fabiano A, Bianchi R and Rezzani R: Atherosclerosis and oxidative stress. Histol Histopathol. 23:381–390. 2008.PubMed/NCBI
10	Stocker R and Keaney JF: Role of oxidative modifications in atherosclerosis. Physiol Rev. 84:1381–1478. 2004. View Article : Google Scholar : PubMed/NCBI
11	Madamanchi NR, Hakim ZS and Runge MS: Oxidative stress in atherogenesis and arterial thrombosis: The disconnect between cellular studies and clinical outcomes. J Thromb Haemost. 3:254–267. 2005. View Article : Google Scholar : PubMed/NCBI
12	Valko M, Rhodes CJ, Moncol J, Izakovic M and Mazur M: Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chem Biol Interact. 160:1–40. 2006. View Article : Google Scholar : PubMed/NCBI
13	Shao B and Heinecke JW: HDL, lipid peroxidation, and atherosclerosis. J Lipid Res. 50:599–601. 2009. View Article : Google Scholar : PubMed/NCBI
14	Lee SE and Park YS: Role of lipid peroxidation-derived α, β-unsaturated aldehydes in vascular dysfunction. Oxid Med Cell Longev. 2013:6290282013. View Article : Google Scholar : PubMed/NCBI
15	Ahmadinejad F, Geir Møller S, Hashemzadeh-Chaleshtori M, Bidkhori G and Jami M-S: Molecular Mechanisms behind Free Radical Scavengers Function against Oxidative Stress. Antioxidants. 6:512017. View Article : Google Scholar
16	Beutler E, Duron O and Kelly BM: Improved method for the determination of blood glutathione. J Lab Clin Med. 61:882–888. 1963.PubMed/NCBI
17	Kadiiska MB, Gladen BC, Baird DD, Germolec D, Graham LB, Parker CE, Nyska A, Wachsman JT, Ames BN, Basu S, et al: Biomarkers of oxidative stress study II: Are oxidation products of lipids, proteins, and DNA markers of CCl4 poisoning? Free Radic Biol Med. 38:698–710. 2005. View Article : Google Scholar : PubMed/NCBI
18	Amatuzio DS, Grande F and Wada S: The cyanmethemoglobin method for hemoglobin determination. Minn Med. 45:378–381. 1962.PubMed/NCBI
19	Cynamon HA, Isenberg JN and Nguyen CH: Erythrocyte malondialdehyde release in vitro: A functional measure of vitamin E status. Clin Chim Acta. 151:169–176. 1985. View Article : Google Scholar : PubMed/NCBI
20	Andersen HR, Nielsen JB, Nielsen F and Grandjean P: Antioxidative enzyme activities in human erythrocytes. Clin Chem. 43:562–568. 1997.PubMed/NCBI
21	Sonet J, Bierla K, Bulteau A-L, Lobinski R and Chavatte L: Comparison of analytical methods using enzymatic activity, immunoaffinity and selenium-specific mass spectrometric detection for the quantitation of glutathione peroxidase 1. Anal Chim Acta. 1011:11–19. 2018. View Article : Google Scholar : PubMed/NCBI
22	Miller NJ, Rice-Evans C, Davies MJ, Gopinathan V and Milner A: A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates. Clin Sci (Lond). 84:407–412. 1993. View Article : Google Scholar : PubMed/NCBI
23	Damy T, Kirsch M, Khouzami L, Caramelle P, Le Corvoisier P, Roudot-Thoraval F, Dubois-Randé JL, Hittinger L, Pavoine C and Pecker F: Glutathione deficiency in cardiac patients is related to the functional status and structural cardiac abnormalities. PLoS One. 4:e48712009. View Article : Google Scholar : PubMed/NCBI
24	Kaur K, Bedi G, Kaur M, Vij A and Kaur I: Lipid peroxidation and the levels of antioxidant enzymes in coronary artery disease. Indian J Clin Biochem. 23:33–37. 2008. View Article : Google Scholar : PubMed/NCBI
25	Pamplona R: Membrane phospholipids, lipoxidative damage and molecular integrity: A causal role in aging and longevity. Biochim Biophys Acta. 1777:1249–1262. 2008. View Article : Google Scholar : PubMed/NCBI
26	Kumar E, Mukherjee R, Senthil R, Parasuraman S and Suresh B: Evaluation of oxidative stress and antioxidant status in patients with cardiovascular disease in rural populations of the nilgiris, South India. ISRN pharmacol. 2012:9410682012. View Article : Google Scholar : PubMed/NCBI
27	Bhat MA, Mahajan N and Gandhi G: Oxidative stress status in coronary artery disease patients. Int J Life Sc Bt Pharm Res. 1:236–243. 2012.
28	Surekha RH, Srikanth BB, Jharna P, Ramachandra RV, Dayasagar RV and Jyothy A: Oxidative stress and total antioxidant status in myocardial infarction. Singapore Med J. 48:137–142. 2007.PubMed/NCBI
29	Amaki T, Suzuki T, Nakamura F, Hayashi D, Imai Y, Morita H, Fukino K, Nojiri T, Kitano S, Hibi N, et al: Circulating malondialdehyde modified LDL is a biochemical risk marker for coronary artery disease. Heart. 90:1211–1213. 2004. View Article : Google Scholar : PubMed/NCBI
30	Serdar Z, Aslan K, Dirican M, Sarandöl E, Yeşilbursa D and Serdar A: Lipid and protein oxidation and antioxidant status in patients with angiographically proven coronary artery disease. Clin Biochem. 39:794–803. 2006. View Article : Google Scholar : PubMed/NCBI
31	Serdar Z, Yeşilbursa D, Dirican M, Sarandöl E and Serdar A: Sialic acid and oxidizability of lipid and proteins and antioxidant status in patients with coronary artery disease. Cell Biochem Funct. 25:655–664. 2007. View Article : Google Scholar : PubMed/NCBI
32	Vnukov VV, Sidorov RV, Milutina NP, Ananyan AA, Gvaldin DY, Sagakyants AB, Shlyk IF and Talalaev EP: Concentration of proinflammatory cytokines, peroxiredoxin-1 and glutathione peroxidase activity in the blood plasma of patients with coronary artery disease undergoing coronary artery bypass grafting. Adv Gerontol. 30:269–275. 2017.(In Russian). PubMed/NCBI
33	Holley AS, Miller JH, Larsen PD and Harding SA: Relationship between glutathione peroxidase, platelet reactivity, and reactive oxygen species in an acute coronary syndrome population. Ann Clin Lab Sci. 46:639–644. 2016.PubMed/NCBI
34	Holley A, Pitman J, Miller J, Harding S and Larsen P: Glutathione peroxidase activity and expression levels are significantly increased in acute coronary syndromes. J Investig Med. 65:919–925. 2017. View Article : Google Scholar : PubMed/NCBI