Many enzyme systems such as glutathione peroxidase (GPx) or superoxide dismutase (SOD) neutralise the oxygen derived free radicals produced during myocardial reperfusion by thrombolysis. Erythrocytic SOD, plasma and erythrocytic GPx and their cofactor selenium, substances reacting with thiobarbituric acid (TBARS) were analysed by repeated sampling between T0 and 48 hours in 24 patients treated by thrombolysis for acute myocardial infarction. Angiographic control was undertaken systematically between 60 and 180 minutes after initiating thrombolytic therapy: 18 patients had a patent vessel and 6 patients had an occluded vessel recanalised in 5 cases by angioplasty. Biological analysis was performed in the 23 patients successfully revascularised by thrombolysis, eventually completed by angioplasty. The plasma GPx decreased non-significantly between T0 and 2 hours from 246.8 +/- 53.3 to 233 +/- 39 U/ml with a significant increase between 2 and 48 hours from 233 +/- 39.2 to 294 +/- 76 U/ml, whereas the erythrocytic GPx rose significantly and constantly between T0 and 48 hours from 34.8 +/- 7.1 to 37.6 +/- 7.5 U/gHb with significant consumption of selenium between T0 and 4 hours from 81.2 +/- 14 to 68.5 +/- 12.6 micrograms/l. The erythrocytic SOD increased significantly between T0 and 48 hours from 318.9 +/- 40.8 to 337 +/- 59 U/gHb. Finally, the analysis of plasma TBARS showed a non-significant rise between T0 and 30 minutes from 1.59 +/- 0.30 to 1.71 +/- 1.43 mm/l with a return to the basic line values after about 2 hours. These results show a significant increase in the activity of enzymes protecting against the liberation of oxygen free radicals, such as erythrocyte or plasma GPx and erythrocyte SOD between T0 and 48 hours with consumption of selenium, cofactor of GPx, and an increase in circulating lipid peroxydes in acute myocardial infarction treated by thrombolysis. They also illustrate the oxidative stress which occurs in this situation.