Fromin vivo models of stroke it is known that ischemia⁄reperfusion indu-ces oxidative stress that is accompanied by deterioration of brain mito-chondria. Previously, we reported that the increase in Ca 2+ induces functional breakdown and morphological disintegration in brain mitochon-dria subjected to hypoxia⁄reoxygenation (H⁄R). Protection by ADP indica-ted the involvement of the mitochondrial permeability transition pore in the mechanism of membrane permeabilization.