Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2007.08.196
Title: Role of calcium and cyclophilin D in the regulation of mitochondrial permeabilization induced by glutathione depletion
Authors: Lu, C. 
Armstrong, J.S. 
Keywords: Antioxidant
BAPTA
Calcium
Cyclophilin D
Diethyl maleate
Glutathione
Mitochondria
Mitochondrial permeability transition
Reactive oxygen species
Redox
Issue Date: 2007
Source: Lu, C., Armstrong, J.S. (2007). Role of calcium and cyclophilin D in the regulation of mitochondrial permeabilization induced by glutathione depletion. Biochemical and Biophysical Research Communications 363 (3) : 572-577. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2007.08.196
Abstract: The mitochondrial permeability transition (MPT) is a calcium and oxidative stress sensitive transition in the permeability of the mitochondrial inner membrane that plays a crucial role in cell death. However, the mechanism regulating the MPT remains controversial. To study the role of oxidative stress in the regulation of the MPT, we used diethyl maleate (DEM) to deplete glutathione (GSH) in human leukemic CEM cells. GSH depletion increased mitochondrial calcium and reactive oxygen species (ROS) levels in a co-dependent manner causing loss of mitochondrial membrane potential (Δψm) and cell death. These events were inhibited by the calcium chelator BAPTA-AM and the antioxidants N-acetylcysteine (NAC) and the triphenyl phosphonium-linked ubiquinone derivative MitoQ. In contrast, the MPT inhibitor cyclosporine A (CsA) and small interference RNA (siRNA) knockdown of cyclophilin D (Cyp-D) were not protective. These results indicate that mitochondrial permeabilization induced by GSH depletion is not regulated by the classical MPT. © 2007 Elsevier Inc. All rights reserved.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/28654
ISSN: 0006291X
10902104
DOI: 10.1016/j.bbrc.2007.08.196
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