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beta-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease
Wan, L; Nie, GJ; Zhang, J; Luo, YF; Zhang, P; Zhang, ZY; Zhao, BL; 张鹏(多); Zhang ZY(张智勇)
2011
发表期刊FREE RADICAL BIOLOGY AND MEDICINE
卷号50期号:1页码:#REF!
通讯作者Zhao, BL (reprint author), Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China.
文章类型Article
摘要Recent studies indicate that the deposition of beta-amyloid peptide (A beta) is related to the pathogenesis of Alzheimer disease (AD); however, the underlying mechanism is still not clear. The abnormal interactions of A beta with metal ions such as iron are implicated in the process of A beta deposition and oxidative stress in AD brains. In this study, we observed that A beta increased the levels of iron content and oxidative stress in SH-SY5Y cells overexpressing the Swedish mutant form of human beta-amyloid precursor protein (APPsw) and in Caenorhabditis elegans A beta-expressing strain CL2006. Intracellular iron and calcium levels and reactive oxygen species and nitric oxide generation significantly increased in APPsw cells compared to control cells. The activity of superoxide dismutase and the antioxidant levels of APPsw cells were significantly lower than those of control cells. Moreover, iron treatment decreased cell viability and mitochondrial membrane potential and aggravated oxidative stress damage as well as the release of A beta 1-40 from the APPsw cells. The iron homeostasis disruption in APPsw cells is very probably associated with elevated expression of the iron transporter divalent metal transporter 1, but not transferrin receptor. Furthermore, the C. elegans with A beta-expression had increased iron accumulation. In aggregate, these results demonstrate that A beta accumulation in neuronal cells correlated with neuronal iron homeostasis disruption and probably contributed to the pathogenesis of AD. (C) 2010 Elsevier Inc. All rights reserved.
关键词Alzheimer disease Neuronal iron metabolism beta-Amyloid peptide Oxidative stress Free radicals
学科领域Biochemistry & Molecular Biology; Endocrinology & Metabolism
DOI10.1016/j.freeradbiomed.2010.10.707
收录类别SCI
WOS类目Biochemistry & Molecular Biology ; Endocrinology & Metabolism
WOS记录号WOS:000286407700013
引用统计
被引频次:57[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.ihep.ac.cn/handle/311005/226308
专题多学科研究中心
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GB/T 7714
Wan, L,Nie, GJ,Zhang, J,et al. beta-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease[J]. FREE RADICAL BIOLOGY AND MEDICINE,2011,50(1):#REF!.
APA Wan, L.,Nie, GJ.,Zhang, J.,Luo, YF.,Zhang, P.,...&张智勇.(2011).beta-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease.FREE RADICAL BIOLOGY AND MEDICINE,50(1),#REF!.
MLA Wan, L,et al."beta-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease".FREE RADICAL BIOLOGY AND MEDICINE 50.1(2011):#REF!.
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