Literature DB >> 30233785

Oxidant and antioxidant status in coronary artery disease.

Abdolhossein Bastani1, Sadegh Rajabi1, Afshin Daliran1, Habibollah Saadat2, Feridoun Karimi-Busheri3.   

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.

Entities:  

Keywords:  acute coronary syndrome; coronary artery disease; glutathione peroxidase; malondialdehyde; oxidative stress

Year:  2018        PMID: 30233785      PMCID: PMC6142042          DOI: 10.3892/br.2018.1130

Source DB:  PubMed          Journal:  Biomed Rep        ISSN: 2049-9434


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