Homocysteine and oxidative stress markers and inflammation in patients with coronary artery disease

Authors:Parameswaran Aparna, Anil Malleshi Betigeri, Palanisamy Pasupathi
Int J Biol Med Res. 2010; 1(4): 125 – 129  |  PDF File

Abstract

Coronary Artery Disease (CAD) is the major cause of mortality and morbidity worldwide. It is associated with various risk factors such as age group (41 – 60 years), male gender, smoking habit and hypertension. The exact pro-oxidant and antioxidant status in patients with CAD is still not clear. This work was undertaken to assess oxidative stress and antioxidant status in patients with CAD and its contribution to the risk of cardiovascular disease. The study population contained 100 subjects divided in two groups, 50 patients with CAD and equal number of age and sex matched healthy subjects were investigated. Lipid peroxidation as evidenced by thiobarbutric acid reactive substances (TBARS) and the status of enzymatic (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamins (vitamin A, E and C), cardiac markers like CK-MB, C-reactive protein (CRP) and homocysteine were determined. The level of plasma and erythrocyte TBARS was markedly increased in the CAD patients when compared to control subjects. The level of enzymic and non-enzymic antioxidant states was significantly decreased in CAD patients when compared to control subjects. CAD is associated with greater than normal lipid peroxidation and with an imbalance in antioxidants’ status. The level of serum homocysteine and CRP were significantly higher in CAD patients than in the controls.The results of our study suggest higher oxygen free radical production, which is evidenced by increased lipid peroxidation and decreased antioxidant states and support to the oxidative stress in coronary artery disease. Increased homocysteine levels and decreased antioxidant capacity may contribute to the increased risk of cardiovascular disease in patients with coronary artery disease. The increased activities of antioxidant enzymes may be a compensatory regulation in response to decreased oxidative stress.