首页> 外文期刊>Biological Trace Element Research >Protective effect of selenium on protein-undernutrition-induced brain damage in rats
【24h】

Protective effect of selenium on protein-undernutrition-induced brain damage in rats

机译:硒对蛋白质营养不良所致大鼠脑损伤的保护作用

获取原文
获取原文并翻译 | 示例
           

摘要

The effect of ad libitum ingestion of selenium (Se) in drinking water (0.15 mg SeO2/L) for 3 wk on the brain weight, total brain protein, glutathione (GSH) level, catalase activity, and lipid peroxidation in the brain of protein-undernourished (PU) rats was investigated, in an attempt to determine whether antioxidants alone can reverse some of the neuropathological changes associated with protein undernutrition in rats. Feeding on a normal diet (16% casein) by well-fed rats or a low-protein diet (5% casein) by PU rats and Se-treated PU rats lasted 14 wk. Setreated PU rats were given Se in drinking water during the last 3 wk of the experiment. Results show that protein undernutrition induced significant reductions (p<0.001) in brain weight, total brain protein, and catalase activity (p<0.05) while it induced a significant increase (p<0.05) in lipid peroxidation when compared with well-nourished rats; but no significant effect was observed for the GSH level. However, the ingestion of Se in drinking water by PU rats for 3 wk resulted in significant increases (p<0.05) in brain weight, catalase activity, and total brain protein but induced a significant reduction (p<0.05) in lipid peroxidation when compared with PU rats given water. The values obtained for Setreated PU rats are comparable with those obtained for well-nourished rats. The GSH level was, however, not affected by Se ingestion. We suggest that Se, by inducing increases in the concentration of certain proteins, including catalase, in the brain, abolished some of the pathological changes associated with protein undermutrition in the brain, and appears as a promising antioxidant in the prevention and management of pro-oxidant-induced brain damage.
机译:连续3周随意摄入硒(0.15 mg SeO2 / L)中的硒对脑重量,总脑蛋白,谷胱甘肽(GSH)水平,过氧化氢酶活性和脂质过氧化的影响对蛋白质营养不良(PU)大鼠的大脑进行了研究,以试图确定单独的抗氧化剂是否可以逆转与蛋白质营养不良有关的某些神经病理变化。喂饱的大鼠以正常饮食(16%酪蛋白)或PU大鼠和Se处理的PU大鼠以低蛋白饮食(5%酪蛋白)为食持续14周。在实验的最后3周内,将SE处理过的PU大鼠的饮用水中添加硒。结果表明,与营养丰富的大鼠相比,蛋白质营养不足导致体重,总脑蛋白和过氧化氢酶活性显着降低(p <0.001),而脂质过氧化显着降低(p <0.05)。 ;但对谷胱甘肽水平没有明显影响。然而,PU大鼠连续3周摄入饮用水中的Se导致脑重量,过氧化氢酶活性和总脑蛋白显着增加(p <0.05),但与脂质过氧化相比,脂质过氧化显着降低(p <0.05)用PU大鼠给水。经处理的PU大鼠获得的值与营养丰富的大鼠获得的值相当。然而,谷胱甘肽水平不受硒摄入的影响。我们认为,硒通过诱导大脑中某些蛋白质(包括过氧化氢酶)的浓度增加,消除了与大脑中蛋白质突变有关的某些病理变化,并且在预防和管理促红细胞生成素中似乎是有希望的抗氧化剂。氧化剂引起的脑损伤。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号