Oxidative stress and inflammatory marker: possible pathogenic role in acute coronary syndrome

ABSTRACT

Acute coronary syndrome [ACS], which comprise unstable angina [UA] and acute myocardial infarction [AMI] are multifactor diseases involving both thrombotic and inflammatory processes. C-reactive protein [CRP] has emerged as independent risk indicator of active atherosclerosis. Reactive oxygen species [ROS] are key mediators of signaling pathways that underlie vascular inflammation in atherogenesis starting from the initiation of fatty streak development through lesion progression to ultimate plaque rupture. CRP directly up-regulate AND[P]H oxidase p22 [phox] and enhance ROS generation. Recently it has been shown that 8-iso-prostaglandin F2 alpha [8-iso-PGF2_] is a specific, chemically stable and quantitative marker of oxidative stress in vivo. It is formed in situ in cell membranes following free radical attack on the arachidonic acid. To counteract the effect of ROS, cells are endowed with a complex antioxidant network that operates to prevent or limit oxidant damage. The present study was designed to investigate the changes of 8-iso-PGF2_, total antioxidant capacity [TAC] and CRP levels in patients with acute coronary syndrome in order to evaluate the role of oxidative stress as well as inflammation in pathogenesis and consequence of the disease. The present study included 30 patients with ACS and 15 healthy, age and sex-matched controls. The patients were divided into two groups; 15 patients with UA and 15 patients with AMI. Serum leuel of 8-iso-PGF2-_ was measured using an ELISA kit Serum CRP and TAC levels was measured by turbidimetric immunoassay and colorimetric methods respectively. Serum levels of both 8-iso-PGF2- _, and CRP were significantly increased in patients compared with control [p<0.05]. TAG showed significant decrease in patients with AMI when compared to controls [p<0.05]. It could be concluded that elevated levels of 8-iso-PGF2-_ and CRP together with decreased TAC level contribute directly and actively to the pathogenesis of ACS. The oxidative stress is likely to either induce or intensify the inflammatory action, and may co-affect with inflammatory factors to accelerate plaque rupture. The evaluation of oxidative stress would enable formulation of specific antioxidant therapy as promising strategy against atherogenesis for an early intervention and better management of the disease