Mitochondrial formation of superoxide has been recognized for a long time: it is believed to be equal to about 3% of total electron flux, although this amount has never been experimentally proven. It is also frequently accepted that ubiquinone is a source of superoxide production in mitochondria. However, comparison of the one-electron reduction potentials of ubiquinones and dioxygen and a great excess of ubiquinone relatively to the other mitochondrial electron carriers suggest that the equilibrium of reaction between ubiquinone and dioxygen must be shifted to the left, i.e. to the semiquinone and not superoxide formation. Therefore, the study of alternative sources of superoxide in mitochondria such as primary dehydrogenases (Forman and Kennedy, 1975) or NADP. radical (de Grey, 2003) seems to be of importance. There is a mutual agreement that the damaging effects of a rather innocuous superoxide are due to its conversion into hydroxyl radicals by the Fenton reaction. However, for deteriorating mitochondrial activity of superoxide probably relevant to mitochondrial aging, its nucleophilic character might be even more important. It has been well documented (but seems quite forgotten) that superoxide is a false "super" oxidant but exclusively active "supernucleophil." Therefore, superoxide can very easily hydrolyze ester phosphate bonds of ATP and effectively suppress oxidative phosphorylation.