Journal of Biological Sciences1727-30481812-5719Asian Network for Scientific Information10.3923/jbs.2004.568.574M. Abd-El GawadHanan M. AbdallahDalaal S. El-AbharHanan 4200444Increasing evidence has suggested an important role for environmental factors such as exposure to pesticides in the pathogenesis of Parkinson`s disease (PD). Because of the potential role of mitochondrial dysfunction in striatal neurodegeneration in PD, rotenone, a potent reversible competitive inhibitor of complex I, was chosen as a possible trigger of Parkinson`s-like syndrome. The loss of dopaminergic neurons in PD, besides the blockade of mitochondrial complexes, augment the formation of free radicals. Therefore, administration of the mitochondrial enhancer coenzyme Q10 (CoQ10), with its known antioxidant activity, may be promising in attenuating the case. Male Wistar albino rats (250-300 g) were allocated into a normal control group, rotenone-induced toxicity group and rotenone + CoQ10-treated group. Rotenone was injected s.c at a dose of 1.5 mg kg-1 every other day for a total of six injections. CoQ10 was administered orally at a dose of 100 mg kg-1 day -1 starting from the first day of rotenone injection and continued thereafter for a total period of 11 days. The striatal biochemical parameters were assessed 24 h after the last rotenone injection. Rotenone resulted in significant decrease in the contents of dopamine (DA), glutamate and reduced glutathione (GSH) accompanied by a marked increase in malondialdehyde (MDA) level and lactate dehydrogenase (LDH) activity. However, no change was observed in the levels of superoxide dismutase (SOD) and nitric oxide (nitrite/nitrate). CoQ10 reduced the elevated levels of MDA and LDH, while restored that of GSH. However, the activity of SOD enzyme was stimulated. 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