Attenuation of cocaine and methamphetamine neurotoxicity by coenzyme Q10

被引:45
作者
Klongpanichapak, Sirirat
Govitrapong, Piyarat
Sharma, Sushil K.
Ebadi, Manuchair
机构
[1] Univ N Dakota, Sch Med & Hlth Sci, Dept Pharmacol Physiol & Therapeut, Grand Forks, ND 58203 USA
[2] Mahidol Univ, Inst Sci & Technol Res & Dev, Neurobehav Biol Ctr, Nakhon Pathom 73170, Thailand
[3] Mahidol Univ, Ctr Neurosci, Bangkok 10400, Thailand
[4] Mahidol Univ, Dept Pharmacol, Fac Sci, Bangkok 10400, Thailand
[5] Univ N Dakota, Dept Pathol, Grand Forks, ND 58203 USA
关键词
cocaine; methamphetamine; dopamine; CoQ(10); complex I; tyrosine hydroxylase; alpha synuclein; F-18-DOPA; drug addiction;
D O I
10.1007/s11064-005-9025-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 F-18-DOPA uptake as determined by high-resolution microPET neuroimaging. Hence exogenous administration of CoQ(10) may provide neuroprotection in drug addiction.
引用
收藏
页码:303 / 311
页数:9
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