An attempt to arrest the aging program by means ofmitochondria-targeted plastoquinone
Vladimir P. Skulachev
Belozersky Institute of Physico-Chemical Biology, Moscow State University,
Russia
E-mail: skulach@belozersky.msu.ru
A concept is developed considering aging as an evolutionfacilitating program which is unnecessary and counterproductive for human and, therefore, should be arrested. To do this, an attempt is undertaken to inactive mitochondria-produced reactive oxygen species (ROS) which seem to mediate execution of the aging program. We synthesized mitochondria-targeted, rechargeable, hydrophobic antioxidant composed of plastoquinone and cation of decyltriphenylphosphonium (SkQ1). It is shown that very low (nmol/kg/day) amounts of SkQ1 increase the lifespan of a fungus (Podospora anserine), invertebrates(Ceriodaphnia affinis and Drosophila melanogaster) and a mammal (mouse). Even more important, in mice SkQ1 abrogates development of such typical traits of senescence as osteoporosis (kyphosis), decrease in resistance to infections, depression, alopecia (!!!!!!!!!

!!!!!!!!!), loss of whiskers, gray hairs, disappearance of regular oestrous cycles, etc. In rats, pretreatment with SkQ1 or its homolog, SkQR1, has favourable effect in the cases of experimental heart arrhythmia, heart and kidney infarction or stroke. In rats, rabbits, cats, dogs and horses, drops of 250 nM SkQ1 prevent development of certain types of cataract, retinopathies and uveitis and in some cases return vision to animals that became blind due to these pathologies. These data are consistent with the assumption that SkQ1 interferes with execution of aging program and is promising in treating some agerelated
diseases.
Sponsored by O.V. Deripaska; for review, see Skulachev, V.P.
Biochemistry (Moscow), 2007, 72, 1385-1396; http://protein.bio.msu.
ru/biokhimiya/contents/v72/pdf/bcm_1385.pdf.