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It has been well established that the actual toxicity of free radical oxygen-species is dependent on the presence of catalytic amounts of free iron in the tissue. Accumulating evidence is present, indicating that for the myocardial tissue damage occurring during reperfusion after ischemic period, oxygen free radicals are partially responsible. It has been demonstrated that superoxide dismutase decreased the ischemic-induced tissue damage. Based on the hypothesis of McCord and coworkers, implying the conversion of heart tissue xanthine dehydrogenase (XDH) to xanthine oxidase (XO) during ischemia and subsequent superoxide (O -2 ) formation during the conversion of the ATP breakdown product(s) (hypo)xanthine to urate, we studied whether XO is able to mobilize free iron from the iron-binding protein ferritin and transferrin. It appeared that XO-mediated O -2 formation is able to release free iron from the intracellular ferritin, but not from extracellular transferrin. Beside this O -2 -dependent iron release and O -2 -independent Fe mobilization could be demonstrated. The latter phenomenon indicates that during the anoxic/ischemic period iron is mobilized from the ferritin. During myocardial reperfusion when XHD is converted to XO and ATP breakdown happens, the previous released iron starts catalyzing the formation of the most potent oxygen free radical, OH- (hydroxyl radical). 2ff7e9595c