Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbrc.2005.09.059
Title: Oltipraz-induced phase 2 enzyme response conserved in cells lacking mitochondrial DNA
Authors: Chua, Y.L.
Zhang, D.
Whiteman, M. 
Armstrong, J.S. 
Boelsterli, U. 
Moore, P.K. 
Keywords: ρ0
Glutathione
Glutathione S-transferase
Mitochondrial permeability transition
mtDNA
Oltipraz
Reactive oxygen species
Issue Date: 2005
Source: Chua, Y.L., Zhang, D., Whiteman, M., Armstrong, J.S., Boelsterli, U., Moore, P.K. (2005). Oltipraz-induced phase 2 enzyme response conserved in cells lacking mitochondrial DNA. Biochemical and Biophysical Research Communications 337 (1) : 375-381. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2005.09.059
Abstract: Oltipraz, a member of a class of 1,2-dithiolethiones, is a potent phase 2 enzyme inducing agent used as a cancer chemopreventive. In this study, we investigated regulation of the phase 2 enzyme response and protection against endogenous oxidative stress in lymphoblastic leukemic parental CEM cells and cells lacking mitochondrial DNA (mtDNA) (ρ0) by oltipraz. Glutathione (GSH) levels (total and mitochondrial) and glutathione S-transferase (GST) activity were significantly increased after pretreatment with oltipraz in both parental (ρ+) and ρ0 cells, and both cell lines were resistant to mitochondrial oxidation, loss of mitochondrial membrane potential, and cell death in response to the GSH depleting agent diethylmaleate. These results show that the phase 2 enzyme response, by enhancing GSH-dependent systems involved in xenobiotic metabolism, blocks endogenous oxidative stress and cell death, and that this response is intact in cells lacking mtDNA. © 2005 Elsevier Inc. All rights reserved.
Source Title: Biochemical and Biophysical Research Communications
URI: http://scholarbank.nus.edu.sg/handle/10635/28887
ISSN: 0006291X
DOI: 10.1016/j.bbrc.2005.09.059
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