Possible protective effect of coenzyme Q-1O against rotenone-induced neurodegeneration in rats

ABSTRACT

Rotenone, a plant extract pesticide, destroys dopamine-producing neurons and causes symptoms of Parkinson's disease in the experimental animals. Thus, this study was conducted to evaluate the neurochemical and histopathological effects of repeated exposure to rotenone and testing the probable preventive effect of coerizyme Q-10 [CoQ-10, a mitochondrial enhancer and antioxidant] in specified rat brain areas. Rotenone was injected subcutaneously at a dose of 2 mg/kg every other day up to six injections for a total period of II days, another group of rats fed with coenzyme Q-10 orally at a dose of 100mg/kg/day, starting from the first day of rotenone injection and continued for a total period of 11 days. A combination of rotenone and coenzyme Q-10 was given to a third group of rats. Dopamine [DA] and norepinephrine [NE] were measured in brain cortex and striatum. The levels of oxidative stress parameters including nitric oxide [NO] [as total nitrite and nitrate] and reduced and oxidized glutathione, the enzymatic activity of total superoxide dismutase [SOD], malondialdehyde [MDA], and protein carbonyls and adenosine triphosphate [ATP] in brain cortex and striatum of the treated animals were determined. Besides, the histopathological changes of the aforementioned brain tissues were studied. Results revealed that subchronic treatment of rotenone significantly reduced the levels of DA, NE and ATP, and increased the levels of nitric oxide, induced lipid and protein peroxidation mirrored by elevated levels of MDA and protein carbonyls, respectively, and induced remarkable histological abnormalities in both brain cortical and striatal regions. Concurrent treatment with CoQ-10 considerably protected the cortex and striatum, through its antioxidant potential, against rotenorie-induced transmitters depletion and oxidative stress. The study might indicate that rotenone induced oxidative stress and mitochondrial dysfunction and that pesticide's effect represents a common, non-specific, brain toxicity and raises a question about the agreeability of rotenone to produce an in-vivo experimental model of Parkinson's disease