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首页> 外文期刊>Nigerian Journal of Physiological Sciences >Modulatory role of vitamins A and E on memory and motor functions of cyanide induced neurotoxicity in adult swiss mice
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Modulatory role of vitamins A and E on memory and motor functions of cyanide induced neurotoxicity in adult swiss mice

机译：维生素A和E对氰化物诱导成人瑞士小鼠神经毒性的记忆和运动功能的调节作用

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Cyanide is a potent neurotoxic substance that can initiate series of intracellular reactions leading to oxidative stress. To evaluate effect of sublethal administration of potassium cyanide (KCN) on sensorimotor functions and long term visuo-spatial learning and memory in adult Swiss mice and possible ameliorative role of vitamins A and E. These vitamins A and E (dietary) are antioxidants that have scavenging properties against free radicals and reactive oxygen species as a result of oxidative stress induced by cyanide. Thirty-five mice weighing between 18-22 g were used for the study. The animals were randomly divided into five groups (n = 7) and exposed to sublethal concentration of potassium cyanide (10% LD50; 1.5 mg/kg). KCN was administered orally while vitamin A (25 mg/kg) and vitamin E (50 mg/kg) were administered intra-peritoneal (IP) once daily for 28 days. Potassium cyanide (KCN) was first administered and after 10 minutes intervals, followed by vitamin A and then E after 5 minutes, vitamin E were administered across the different treatment groups. Mice were examined for signs of toxicity. Vitamins pre-treatment ameliorated toxic signs. In the dynamics of wire grid, coat hanger and stationary beam test, the latency to fall in weeks 2 and 4 were statistically significant. In acquisition and retention, using elevated plus maze (EPM), KCN treated group recorded high transfer latencies in seconds (50.40±1.72 secs) and (57.60±0.93 secs) as compared to group IV (29.40±0.68 secs; 5.60±0.60 secs). Cyanide is a neurotoxin that affects motor functions with progressive decline in motor strength and coordination. KCN affects acquisition and retention memory while pre-treatment with antioxidant vitamins A and E ameliorated these deficits.
机译：氰化物是一种有效的神经毒性物质，可以引发一系列导致氧化应激的细胞内反应。为了评估氰化钾（KCN）对亚磷酸钾（KCN）的影响以及成人瑞士小鼠中的长期助理空间学习和记忆的影响，以及维生素A和E.这些维生素A和E（膳食）是具有抗氧化剂的可能性作为氰化物诱导的氧化应激的氧化胁迫，清除自由基和反应性氧物质的清除性能。在18-22g之间使用35只小鼠用于研究。将动物随机分为五组（n = 7）并暴露于氰化钾的亚致苯浓度（10％LD50; 1.5mg / kg）。口服kcn施用，而维生素a（25mg / kg）和维生素E（50mg / kg）每天一次施用一次腹膜内（IP）28天。首次施用氰化钾（KCN），并在10分钟后进行一次施用，然后在5分钟后进行维生素A，然后e e，在不同的处理基团上施用维生素E.检查小鼠的毒性迹象。维生素预处理改善有毒迹象。在丝网，涂层衣架和固定光束试验的动态中，在第2周和4周内下降的潜伏期在统计上显着。在采集和保留时，使用升高的加迷宫（EPM），KCN处理组以秒（50.40±1.72秒）以秒（50.40±1.72秒）记录高转移延迟（57.60±0.93秒），与第IV组相比（29.40±0.68秒; 5.60±0.60秒）。氰化物是一种神经毒素，影响电机功能，具有电机强度和协调的逐步下降。 KCN影响采集和保留记忆，同时用抗氧化维生素A预处理，e改善这些缺陷。

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