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FRBM:维生素D水平较低或引发个体大脑损伤

来源:生物谷 2013-12-03 23:57

2013年12月3日 讯 /生物谷BIOON/ --近日,来自肯塔基大学的研究者通过研究表明,低维生素D的饮食可以引发个体出现脑部损伤,相关研究刊登于国际杂志Free Radical Biology and Medicine上。

除了具有保护骨骼健康的作用外,新的研究证据揭示,维生素D对于其它器官和组织也非常重要,包括脑部等。文章中,研究者表示,对中年大鼠长达数月喂食低维生素D饮食会导致其脑部出现自由基损伤,而且也会使得大脑中许多不同的蛋白质被损伤。与此同时这些大鼠在学习和记忆能力上均出现了明显的认知力降低的表现。

Allan Butterfield教授说道,维生素D缺失在老年个体中表现尤为明显,我们的研究就揭示了低水平的维生素D为何会严重影响中老年个体大脑中的氧化状态;而血清中充足的维生素D对于阻断大脑的自由基损伤以及更为恶劣的疾病则非常重要。

此前研究揭示低水平的维生素D和阿尔兹海默氏症直接相关,而且也和某些癌症、心脏疾病直接相关;如今人们的维生素D摄入水平依然很低,研究者建议人们多食用一些富含维生素D的食物来补充维生素D,这样对于保护个体的大脑健康非常有必要。(生物谷Bioon.com)

Dietary vitamin D deficiency in rats from middle to old age leads to elevated tyrosine nitration and proteomics changes in levels of key proteins in brain: Implications for low vitamin D-dependent age-related cognitive decline

Jeriel T.R. Keeneya, Sarah Förstera, Rukhsana Sultanaa, Lawrence D. Brewerb, Caitlin S. Latimerb, Jian Caic, Jon B. Kleinc, Nada M. Porterb, D. Allan Butterfield

In addition to the well-known effects of vitamin D (VitD) in maintaining bone health, there is increasing appreciation that this vitamin may serve important roles in other organs and tissues, including the brain. Given that VitD deficiency is especially widespread among the elderly, it is important to understand how the range of serum VitD levels that mimic those found in humans (from low to high) affects the brain during aging from middle age to old age. To address this issue, 27 male F344 rats were split into three groups and fed isocaloric diets containing low (100 IU/kg food), control (1000 IU/kg food), or high (10,000 IU/kg food) VitD beginning at middle age (12 months) and continued for a period of 4–5months. We compared the effects of these dietary VitD manipulations on oxidative and nitrosative stress measures in posterior brain cortices. The low-VitD group showed global elevation of 3-nitrotyrosine compared to control and high-VitD-treated groups. Further investigation showed that this elevation may involve dysregulation of the nuclear factor κ-light-chain enhancer of activated B cells (NF-κB) pathway and NF-κB-mediated transcription of inducible nitric oxide synthase (iNOS) as indicated by translocation of NF-κB to the nucleus and elevation of iNOS levels. Proteomics techniques were used to provide insight into potential mechanisms underlying these effects. Several brain proteins were found at significantly elevated levels in the low-VitD group compared to the control and high-VitD groups. Three of these proteins, 6-phosphofructokinase, triose phosphate isomerase, and pyruvate kinase, are involved directly in glycolysis. Two others, peroxiredoxin-3 and DJ-1/PARK7, have peroxidase activity and are found in mitochondria. Peptidyl–prolyl cis–trans isomerase A (cyclophilin A) has been shown to have multiple roles, including protein folding, regulation of protein kinases and phosphatases, immunoregulation, cell signaling, and redox status. Together, these results suggest that dietary VitD deficiency contributes to significant nitrosative stress in brain and may promote cognitive decline in middle-aged and elderly adults.

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