Oxidative DNA Damage and Antioxidant Defense after Reperfusion in Acute Myocardial Infarction

PURPOSE: Myocardial damage mediated by oxidative stress during acute myocardial infarction (MI) has been suggested as an obstructive factor on recovery after an MI. 8-Hydroxydeoxyguanosine (8-OHdG) is a marker for oxidative DNA damage; superoxide dismutase (SOD) and glutathione peroxidase (G-Px) are major antioxidant enzymes. We determined changes in the plasma level of 8-OHdG and activities of SOD and G-Px in patients with MI and examined the relations between those changes and other cardiac markers. METHODS: Blood samples were taken at the beginning of the therapy, on the third day of hospitalization, and on the day patients were discharged home. Plasma level of 8-OHdG and SOD and G-Px activities were measured by enzyme-linked immunosorbent assay and spectrophotometric kits, respectively. RESULTS: 8-Hydroxydeoxyguanosine level at the beginning of the therapy was found to be decreased on the third day of therapy and on the day patients were discharged home. With respect to the treatment way, 8-OHdG level was found to be slightly decreased on the third day of therapy and then remained stable in the group treated with thrombolytic agents. However, 8-OHdG level was found to be sharply decreased on the third day of therapy in the group that underwent primary percutaneous transluminal coronary angioplasty. No significant relations were determined between those measured parameters and serum levels of cardiac markers. CONCLUSION: Although not correlated with other cardiac markers, plasma level of 8-OHdG shows a decrease after reperfusion therapy in patients with MI, and primary percutaneous transluminal coronary angioplasty seems much more effective than thrombolytic therapy for providing a low level of 8-OHdG.