Please use this identifier to cite or link to this item:
|Title:||Role of calcium and cyclophilin D in the regulation of mitochondrial permeabilization induced by glutathione depletion||Authors:||Lu, C.
Mitochondrial permeability transition
Reactive oxygen species
|Issue Date:||2007||Citation:||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
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Oct 22, 2021
WEB OF SCIENCETM
checked on Oct 13, 2021
checked on Oct 14, 2021
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.