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KEY WORDS: myocardial infarction, antioxidant therapy, activation of lipid peroxidation.Ischemic damage to the tissues is accompanied by marked activation of free-radical lipid peroxidation (LPO) [3]. Activation of LPO also is observed during the formation of a myocardial infarct (MI) [5]. One cause of the intensification of LPO in infarction may be the decrease in activity of protective "antioxidant" enzyme systems [9], which detoxicate active forms of oxygen and lipid peroxides --superoxide dismutase (DOS), glutathione peroxidases (GP), and glutathione-S-transferases (GT) --in the ischemic and infarcted zone of the myocardium, discovered previously by the present writers [6] and others [2, i0]. A marked antinecrotic affect of natural and synthetic antioxidants has been demonstrated [5, ii].Considering that antioxidants can exhibit their action ~n u~uo indirectly through a change in the activity of "antioxidant" enzyme systems [7], it was decided to study the effect of the synthetic antioxidant dibunol (ionol, 2,6-di-tert-butyl-4-methylphenol), approved for pharmacologic use, on limitation of the zone of MI produced by coronary occlusion in rats and on DOS, GP, and GT activity in the heart muscle. EXPERIMENTAL METHODExperiments were carried out on I00 male Wistar rats weighing 180 • 20 g. MI was produced by ligation of the left coronary artery 2 mm below the level where it crosses the left border of the infundibulum at its base [4]. Operations were performed under endotracheal ether anesthesia.Ionol was administrered perorally through a tube in the form of a solution in sunflower oil in doses of 40, 80, and 120 mg/kg 24 h before the operation, and again 2 h before application of the ligature and daily for the next 7 days. Rats with MI receiving the solvent alone (sunflower oil, 1 ml/kg) served as the control. The animals were killed on the 7th day after coronary occlusion at the stage of scar formation [6]. The infarct was verified macroscopically by the presence of a zone of necrosis and a postinfarct scar. The presence of ischemia and an infarct was determined by characteristic changes in the ECG (elevation of ST and deepening of the Q wave) in three standard leads.The dimensions of MI were measured by the method [i0] in the writers' modification.The heart was cut through the zone of the

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