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Effects of Mitochondrial Antioxidant SkQ1 on Biochemical and Behavioral Parameters in a Parkinsonism Model in Mice

V. V. Pavshintsev1,2*, L. S. Podshivalova2, O. Y. Frolova1, M. V. Belopolskaya1, O. A. Averina2, E. A. Kushnir1, N. V. Marmiy1, and M. L. Lovat1,2

1Institute of Mitoengineering, Lomonosov Moscow State University, 119234 Moscow, Russia; E-mail: vsevolodpav@mail.ru

2Lomonosov Moscow State University, Faculty of Biology, 119234 Moscow, Russia

* To whom correspondence should be addressed.

Received July 28, 2017; Revision received August 23, 2017
According to one hypothesis, Parkinson’s disease pathogenesis is largely caused by dopamine catabolism that is catalyzed on mitochondrial membranes by monoamine oxidase. Reactive oxygen species are formed as a byproduct of these reactions, which can lead to mitochondrial damage followed by cell degeneration and death. In this study, we investigated the effects of administration of the mitochondrial antioxidant SkQ1 on biochemical, immunohistochemical, and behavioral parameters in a Parkinson-like condition caused by protoxin MPTP injections in C57BL/6 mice. SkQ1 administration increased dopamine quantity and decreased signs of sensory-motor deficiency as well as destruction of dopaminergic neurons in the substantia nigra and ventral tegmental area in mice with the Parkinson-like condition.
KEY WORDS: Parkinson’s disease, MPTP, mitochondrial antioxidants, SkQ1, sensorimotor deficiency, dopaminergic neurons

DOI: 10.1134/S0006297917120100