Rotenone-induced parkinson's like disease: Modulating role ofcoenzyme Q10

Increasing evidence has suggested an important role forenvironmental factors such as exposure to pesticides in thepathogenesis of Parkinson's disease (PD). Because of the potentialrole of mitochondrial dysfunction in striatal neurodegeneration in PD,rotenone, a potent reversible competitive inhibitor of complex I, waschosen as a possible trigger of Parkinson's-like syndrome. The lossof dopaminergic neurons in PD, besides the blockade of mitochondrialcomplexes, augment the formation of free radicals. Therefore,administration of the mitochondrial enhancers coenzyme Q10 (CoQ10),with its known antioxidant activity, may be promising in attenuatingthe case. Male Wistar albino rats (250-300 g) were allocated into anormal control group, rotenone-induced toxicity group and rotenone+ CoQ10-treated group. Rotenone was injected s.c at a dose of 1.5 mgkg-1 every other day for a total of six injections. CoQ10 wasadministered orally at a dose of 100 mg kg-1 day-1 starting from thefirst day of rotenone injection and continued thereafter for a totalperiod of 11 days. The striatal biochemical parameters were assessed24 h after the last rotenone injection. Rotenone resulted insignificant decrease in the contents of dopamine (DA), glutamate andreduced glutathione (GSH) accompanied by a marked increase inmalondialdehyde (MDA) level and lactate dehydrogenase (LDH)activity. However, no change was observed in the levels ofsuperoxide dismutase (SOD) and nitric oxide (nitrite/nitrate). CoQ10reduced the elevated levels of MDA and LDH, while restored that ofGSH. However, the activity of SOD enzyme was stimulated. Inconclusion, this study indicated the role of CoQ10 in ameliorating theoxidative stress associated with PD, but it was not capable ofovercoming the whole negative effects of rotenone. Therefore, newapproaches besides providing antioxidants that offer neuroprotectionof striatal dopaminergic neurons in PD are still in need.