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Mitochondrial targeting of quinones: therapeutic implications.

Review article
Authors Helena M Cochemé
Geoffrey F Kelso
Andrew M James
Meredith F Ross
Jan Trnka
Thabo Mahendiran
Jorge Asin-Cayuela
Frances H Blaikie
Abdul-Rahman B Manas
Carolyn M Porteous
Victoria J Adlam
Robin A J Smith
Michael P Murphy
Published in Mitochondrion
Volume 7 Suppl
Pages S94-102
ISSN 1567-7249
Publication year 2007
Published at Institute of Biomedicine
Pages S94-102
Language en
Keywords Administration, Oral, Animals, Cations, Cell Membrane, metabolism, Humans, Membrane Potential, Mitochondrial, Membrane Potentials, Mitochondria, metabolism, Mitochondrial Diseases, therapy, Models, Biological, Models, Chemical, Organophosphorus Compounds, metabolism, Oxygen, metabolism, Quinones, chemistry, Ubiquinone, analogs & derivatives, metabolism
Subject categories Chemical Sciences, Chemistry


Mitochondrial oxidative damage contributes to a range of degenerative diseases. Ubiquinones have been shown to protect mitochondria from oxidative damage, but only a small proportion of externally administered ubiquinone is taken up by mitochondria. Conjugation of the lipophilic triphenylphosphonium cation to a ubiquinone moiety has produced a compound, MitoQ, which accumulates selectively into mitochondria. MitoQ passes easily through all biological membranes and, because of its positive charge, is accumulated several hundred-fold within mitochondria driven by the mitochondrial membrane potential. MitoQ protects mitochondria against oxidative damage in vitro and following oral delivery, and may therefore form the basis for mitochondria-protective therapies.

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