Modulatory Role Of Vitamins A And E On Learning Memory Motor Strength And Coordination Of Cyanide Induced Neurotoxicity In Albino Mice

Background: cyanide is a potent neurotoxic substance that can initiate series of intracellularreactions leading to oxidative stress. Objective: To evaluate effect of sublethal administration ofKCN on motor functions, visuo-spatial learning and memory. Some biochemical parameterswhich include brain malondialdehyde concentration, superoxide dismutase, catalase andacetylcholinesterase activities in adult swiss albino mice and possible ameliorative roles ofvitamins A and E. Methods: Thirty five adult swiss albino mice weighing between 18-22g wereused. In each group served as subjects for this study. An acute toxicity study was carried out andLD50 was calculated as 15mg/kg. The animals were randomly divided into five groups (n = 7)and exposed to sublethal concentration of potassium cyanide (10% LD50; 1.5 mg/kg). Thegroupings were as follows; group I (control received 10 ml deionised water), group II (1.5mg/kgKCN), group III (1.5mg/kg KCN + 25mg/kg vitamin A), group IV (1.5mg/kg KCN + 50mg/kgvitamin E) and group V (1.5mg/kg KCN + 25mg/kg vitamin A + 50mg/kg). The animals werefed for 28 days during which neurobehavioral tests using different paradigms was carried outprior to sacrifice and isolation of tissues for biochemical assays. During the study period, Micewere examined for signs of toxicity. Results: From the results obtained from this study, itsuggests that motor strength was considerably reduced in the KCN treated group as compared tothe vitamins groups. Group2 displayed hypolocomotion on the stationary beam in week 4(15.8±0.58) while group III recorded decrease in transfer latencies to traverse the beam in week4 (3.20±0.58). In acquisition and retention, using EPM, group II recorded an increase in transferlatencies (50.40±1.72) and (57.60±0.93) as compared to group IV (29.40±0.68; 5.60±0.60), micespent more time in the open arms than in the closed arms. Increase in MDA concentrationinduced by KCN (3.35±0.19) which is an index of lipid peroxidation was mitigated whenadministered with vitamins A and E (1.82±0.21). Brain SOD activity was significantly (p<0.05)decreased in group2 (1.30±0.27) as compared to group V (2.78±0.10). Brain acetylcholinesteraseactivity as a biomarker in cyanide toxicity was increased in group II (32.10±0.90) as compared togroup III (14.80±0.86). Conclusion:the study suggests that motor deficits and cognitiveimpairments were correlated with cyanide induced neurotoxicity with increased MDAconcentration levels and decreased antioxidant enzymes while the ameliorative effects ofvitamins A and E may be due to the inhibition of free radicals overproduction and maintenanceof antioxidant defence mechanisms.

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