Wistar rats, fed control or vitamin E-supplemented diet, were subjected to oxidative stress by a ten day treatment with daily intraperitoneal dose of tert-butyl hydroperoxide (TBHP) (0.1 mumol/100 g body weight). The effectiveness of both diet and hydroperoxide treatment was established by determining the antioxidant capacity of blood, liver, and heart with an enhanced luminescence method. While the diet addition of vitamin E increased the antioxidant capacity of all the tissues in treated and untreated animals, the hydroperoxide treatment failed to decrease liver antioxidant capacity in control diet fed animals. The effect of the reiterated production of free radicals on electrophysiological properties of myocardium was determined by studying the heart rate in vivo and the time course of the surface electrical activity in papillary muscle fibers in vitro. In vivo, a significant tachycardia was found only in TBHP-treated, normal diet fed rats. The duration of action potential, recorded in Krebs' solution at 26 degrees C, was not affected by diet in untreated animals but was modified by hydroperoxide treatment in a diet-dependent way: shortened in normal diet-fed rats and lengthened in vitamin E-supplemented diet-fed rats. On the basis of analogies with the results of electrophysiological recordings on different preparations subjected to oxidative stress in vitro, we suggest that the changes of action potential duration might depend on relative levels of added pro-oxidant and cell antioxidants.