Long-Term Vitamin E-Deficient Mice Exhibit Cognitive Dysfunction via Elevation of Brain Oxidation
Long-Term Vitamin E-Deficient Mice Exhibit Cognitive Dysfunction via Elevation of Brain Oxidation
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DOI：
10.3177/jnsv.61.362
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发表时间：
2015-10-01
影响因子：
1.6
通讯作者：
Urano, Shiro
中科院分区：
文献类型：
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作者：
Fukui, Koji;Nakamura, Keisuke;Urano, Shiro
维生素 E 抑制活组织中的氧化过程。我们通过喂养缺乏维生素E的饮食来培育缺乏维生素E的小鼠，以验证慢性维生素E缺乏对认知功能的影响。我们使用莫里斯水迷宫任务测量了 5 天的认知功能，以及离散大脑区域的抗氧化酶活性和脂质过氧化，以及血清总胆固醇含量。使用 3 个月和 6 个月大的维生素 E 缺乏小鼠和年龄匹配的对照小鼠。此外，使用24个月大的小鼠作为老年模型。在 3 个月大的小鼠中，与年龄匹配的对照组相比，维生素 E 缺乏（短期维生素 E 缺乏）组的认知功能显着受损。尽管3个月大的小鼠大脑皮层、小脑和海马中的脂质过氧化产物没有显着差异，但与年龄匹配的对照组相比，6个月大的维生素E缺乏（长期维生素E缺乏）小鼠的水平显着升高。与相应年龄匹配的对照组相比，短期和长期缺乏维生素 E 的小鼠的血清胆固醇含量也显着增加。这些结果表明，慢性维生素 E 缺乏可能会缓慢加速大脑氧化。因此，即使在正常条件下，也可能需要监测维生素 E 浓度，以预防认知功能障碍的风险。
Vitamin E inhibits oxidative processes in living tissues. We produced vitamin E-deficient mice by feeding them a vitamin E-deficient diet to verify the influence of chronic vitamin E deficiency on cognitive function. We measured cognitive function over a 5-d period using the Morris water maze task, as well as antioxidant enzyme activity and lipid peroxidation in discrete brain regions, and total serum cholesterol content. Three- and six-mo-old vitamin E-deficient and age-matched control mice were used. In addition, 24-mo-old mice were used as an aged-model. In the 3-mo-old mice, cognitive function in the vitamin E-deficient (short-term vitamin E-deficient) group was significantly impaired compared to age-matched controls. Although the lipid peroxidation products in the cerebral cortex, cerebellum and hippocampus did not significantly differ in 3-mo-old mice, the levels in the 6-mo-old vitamin E-deficient (long-term vitamin E-deficient) mice were significantly increased compared to age-matched controls. Serum cholesterol content was also significantly increased in the short- and long-term vitamin E-deficient mice compared to their respective age-matched controls. These results indicate that chronic vitamin E deficiency may slowly accelerate brain oxidation. Thus, vitamin E concentrations may need to be monitored in order to prevent the risk of cognitive dysfunction, even under normal conditions.