Cyclical mitochondrial ΔΨM fluctuations linked to electron transport, F0F1 ATP-synthase and mitochondrial Na+/Ca+2 exchange are reduced in Alzheimer's disease cybrids

被引：30

作者：

Thiffault, C ^{[1
]}

Bennett, JP ^{[1
]}

机构：

[1] Univ Virginia, Dept Neurol, Ctr Study Neurodegenerat Dis, Charlottesville, VA 22908 USA

来源：

MITOCHONDRION | 2005年 / 5卷 / 02期

关键词：

mitochondria; flickering; cybrid; Alzheimer's disease;

D O I：

10.1016/j.mito.2004.12.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Reduced complex IV, increased oxidative stress and beta amyloid peptide secretion in Alzheimer's disease (AD) can be replicated in cybrid models. We characterized cyclical mitochondrial Delta Psi(M) fluctuations ('flickering') in neuroblastoma cells and AD/CTL cybrids. Flickering was blocked by ATP-synthase inhibition, was not observed in rho(0) cells and was not blocked by antioxidant treatment. Flickering was not affected by the Ca+2 uniporter antagonist Ru360 but was eliminated by BAPTA or CGP37137 blockade of the mitochondrial Na+/Ca+2 exchanger. AD cybrid mitochondria showed reduced flickering. Flickering seems to represent coupling of Delta Psi(M) to F0F1 ATP-synthase; reduction of flickering in AD cybrids suggests dysfunction of this coupling. (c) 2005 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

引用

页码：109 / 119

页数：11

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