Myeloperoxidase, protein carbonyls and oxidative stress in coronary artery disease

Abstract

ObjectiveOxidative stress and inflammation play important roles in the pathogenesis of coronary artery disease (CAD). Myeloperoxidase (MPO) produced by circulating neutrophils plays an important role in both processes of inflammation and oxidative stress. MPO generates reactive oxygen species which cause oxidative damage to cellular lipids and proteins. Generation and accumulation of oxidative damage plays an proatherogenic role initiating a cascade of damaging cellular changes. This study was designed to evaluate the association of MPO with oxidative stress and to assess MPO as a predictor of CAD. Methods and resultsThirty patients diagnosed with CAD following angiography along with thirty age matched healthy controls were taken into the study. CAD cases had significantly higher triglyceride (p=0.012), lower HDL cholesterol, higher oxidative stress markers malondialdehyde (MDA), protein carbonyl content (PCO), and MPO levels and lower antioxidant ferric reducing ability of plasma (FRAP) levels in CAD patients when compared to controls (p<0.001). The oxidant markers were found to have good sensitivity and specificity at cut off values of MPO 106.25IU/L, PCO 0.250nmol/mg of protein and MDA 1.8μmol/L. MPO was found to be a significant predictor of CAD. ConclusionOur study shows that an increase in MPO levels is associated with oxidative stress and MPO is also observed to be a significant predictor of CAD.