FORMATION AND DAMAGING EFFECTS OF SUPEROXIDE IN MITOCHONDRIA: RELEVANCE TO MITOCHONDRIAL AGING
I.B. Afanas'ev
Vitamin Research Institute, Nauchny pr.14A, Moscow 117820, Russia
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.
Key words:
superoxide, mitochondria, aging
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