Free radicals are highly cytotoxic to the heart and are involved in ischemia/reperfusion injury. In this study, we tested the ability of taurine to neutralize the deleterious effects of free radicals generated ex vivo and in vitro. Taurine was added at a concentration of 0.1 mM to the drinking water of experimental rats during 6 months. The animal hearts were then isolated and submitted to regional ischemia and reperfusion; ventricular fibrillation was significantly reduced as compared to a control group of non-treated animals. Moreover, at a concentration of 1 mM, taurine provided significant cardio-protection against the deleterious effect of free radicals generated by the electrolysis of Krebs-Henseleit buffer. When isolated hearts were perfused with electrolysed buffer, extensive fiber necrosis occurred, as observed by staining with nitro blue tertrazolium, a soluble dye which yields a dark blue formazan stain in the presence of reducing agents This stain was barely detectable when taurine was added to the perfusing electrolysed buffer. To further understand the protecting mechanism of taurine, we used xanthine-xanthine-oxidase as a superoxide (O2-) generating system and monitored the O2- through yield O2--dependent cytochrome c reduction. We demonstrated that taurine did not affect this system, which indicated that it did not scavenge O2- directly. On the other hand, taurine inhibited the auto-oxidation of adrenaline to adrenochrome at pH 7.8 where this auto-oxidation is O2--independent and superoxide dismutase insensitive. We thus conclude that taurine acts as a potent, but non-specific, scavenger of free radicals that cause heart damage and protects against reperfusion-induced ventricular