Attenuation of Cocaine and Methamphetamine
Neurotoxicity by Coenzyme Q(10)

Klongpanichapak S, Govitrapong P, Sharma SK, Ebadi M.
Department of Pharmacology, Physiology and Therapeutics,
School of Medicine & Health Sciences,
University of North Dakota,
501 North Columbia Road,
Grand Forks, ND, 58203, USA,
[email protected].
Neurochem Res. 2006 May 4


The neurotoxic effects of cocaine and methamphetamine (METH) were studied in mice brain with a primary objective to determine the neuroprotective potential of coenzyme Q(10) (CoQ(10)) in drug addiction. Repeated treatment of cocaine or METH induced significant reduction in the striatal dopamine and CoQ(10) in mice. Cocaine or METH-treated mice exhibited increased thiobarbituric acid reactive substances (TBARs) in the striatum and cerebral cortex without any significant change in the cerebellum. Complex I immunoreactivity was inhibited in both cocaine and METH-treated mice, whereas tyrosine hydroxylase (TH) immunoreactivity was decreased in METH-treated mice and increased in cocaine-treated mice. Neither cocaine nor METH could induce significant change in alpha-synuclein expression at the doses and duration we have used in the present study. CoQ(10) treatment attenuated cocaine and METH-induced inhibition in the striatal (18)F-DOPA uptake as determined by high-resolution microPET neuroimaging. Hence exogenous administration of CoQ(10) may provide neuroprotection in drug addiction.

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