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Introduction. Mercury is one of the most hazardous environmental contaminants to living organisms and the central nervous system has been shown to be the main target. Objective. The present work was aimed at evaluating the effect of ascorbic acid on mercury chloride-induced changes on the cerebellar cortex of adult Wistar rats. Material and method. Thirty Wistar rats of average weight of 200g and were randomly divided into 6 groups of 5 rats each. The animals in Group 1 (control) were administered with distilled water, Groups 2 and 3 were administered with 52mg/kg and 26.25mg/kg body weight of HgCl respectively while Groups 4 and 5 were administered with 52mg/kg of HgCl and 5mg/kg of ascorbic acid and 26.25gm/kg of HgCl and 5mg/kg of ascorbic acid respectively, while Group 6 was administered with 5mg/kg of ascorbic acid. The administration was through oral route, daily for 3 weeks. Results. The result of the biochemical parameters showed a significant increase (P < 0.05) on the mean SOD and LPO values after the administration of mercury chloride and Ascorbic acid. Histological observation of the cerebellar cortex, showed normal histo-morphology in Groups 1 and 6 while, the cerebellum in Groups 2, 3, 4 and 5 showed some degenerative, necrotic and cellular changes. Conclusion. However, ascorbic acid administration has shown to ameliorate the induced degenerative changes in the cerebellum caused by mercury chloride toxicity in Wistar rats.

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The correlations of reduced glutathione (GSH) and glutathione peroxidase (GPx) levels with biochemical markers of liver and kidney damage in Trypanosoma brucei brucei infection were studied in rats. Forty adult male rats divided into 2 groups of control and infected were used. Infected rats were inoculated intraperitoneally with 1.0 ml of blood at concentration of 1 x 106 trypanosomes per ml. Serum and tissue samples were collected on days 0, 3, 5 and 7 post-infection (pi) for biochemical analyses. Serum GPx activity had a significant (p < 0.05) positive correlations with liver (r = 0.96) and kidney GSH (r = 0.93) levels. All the measured serum parameters had significant (p < 0.05) negative correlations with serum GPx activity. In conclusion infection of rats with T. brucei brucei caused a decrease in the serum GPx activities and organ GSH levels with increasing parasitaemia and duration of the infection.