ABSTRACT
Paraquat [PQ] belongs to a class of agricultural chemicals known to impact the dopaminergic system adversely causing severe neurotoxicity. PQ was suggested to contribute in the pathogenesis of many neurological disorders including Parkinson's disease. So, the present study aimed to examine the toxic alterations in brain tissue, following sub-chronic treatment with PQ [20 mg/kg, i.p., once weekly for 6 weeks].Three different types of experiments were carried out including behavioral, neurochemical and histopathological ones. Alterations of motor behavioral patterns were examined by testing the locomotor activity using the open field test and the movement coordination using the rotarod apparatus. Changes in brain dopamine [DA] and norepinephrine [NE] contents as well as histopathological examination of brain tissues were accomplished. The possible protective potentials of deprenyl [10 mg/kg; i.p.], quercetin [50 mg/kg; p.o.], green tea extract [1 mg/kg; p.o.] or malt extract [625 mg/kg; p.o.] against sub-chronic PQ-induced neurotoxicity in rats were examined. Results showed that PQ significantly reduced locomotive and motor behaviors. It also provoked remarkable brain damage noted by significant decreases in brain DA as well as NE contents. Furthermore, histopathological examination of PQ-treated brain sections revealed localized focal necrosis and severe loss of neurons. Daily treatment with deprenyl, quercetin and extracts of green tea or malt for 6 weeks significantly ameliorated most of the behavioral, neurochemical and histopathological changes induced by PQ; effects of malt extract being more pronounced. The present results suggest that sub-chronic PQ administration triggers processes characteristic of early stages of dopaminergic neuron degeneration and activates compensatory mechanisms involving both the dopaminergic and noradrenergic transmissions. Considering the present behavioral studies, neurochemical analysis and histopathological observations, one can conclude that the used agents could be of therapeutic potentials in protection against PQ- induced neurotoxicity