Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.biocel.2004.05.018
Title: β-Phenylethyl isothiocyanate mediated apoptosis; Contribution of Bax and the mitochondrial death pathway
Authors: Rose, P. 
Armstrong, J.S. 
Chua, Y.L.
Whiteman, M. 
Ong, C.N. 
Keywords: β-phenylethyl isothiocyanate
BA
Bongkrekic acid
CsA
cyclosporine A
glutathione
GSH
mBCl
mitochondrial membrane potential
mitochondrial permeability transition pore
MMP
monochlorobimane
MPT
PEITC
Rh-123
rhodamine-123
Tfz
TMRM
trifluoperazine
Issue Date: 2005
Source: Rose, P.,Armstrong, J.S.,Chua, Y.L.,Whiteman, M.,Ong, C.N. (2005). β-Phenylethyl isothiocyanate mediated apoptosis; Contribution of Bax and the mitochondrial death pathway. International Journal of Biochemistry and Cell Biology 37 (1) : 100-119. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biocel.2004.05.018
Abstract: The initiating events that lead to the induction of apoptosis mediated by the chemopreventative agent β-phenyethyl isothiocyanate (PEITC) have yet to be elucidated. In the present investigation, we examined the effects of PEITC on mitochondrial function and apoptotic signaling in hepatoma HepG2 cells and isolated rat hepatocyte mitochondria. PEITC induced a conformational change in Bax leading to its translocation to mitochondria in HepG2 cells. Bax accumulation was associated with a rapid loss of mitochondrial membrane potential (Δψm), impaired respiratory chain enzymatic activity, release of mitochondrial cytochrome c and the activation of caspase-dependent cell death. Caspase inhibition did not prevent Bax translocation, the release of cytochrome c or the loss of Δψ m, but blocked caspase-mediated DNA fragmentation and cell death. To determine whether PEITC dependent Bax translocation caused loss of Δψm by the activation of the mitochondrial permeability transition (MPT), we examined the effects of PEITC in isolated rat hepatocyte mitochondria. Interestingly, PEITC did not induce MPT in isolated rat mitochondria. Accordingly, using pharmacological inhibitors of MPT namely cyclosporine A, trifluoperazine and Bongkrekic acid we were unable to block PEITC mediated apoptosis in HepG2 cells, this suggesting that mitochondrial permeablisation is a likely consequence of Bax dependent pore formation. Taken together, our data suggest that mitochondria are a key target in PEITC induced apoptosis in HepG2 cells via the pore forming ability of pro-apoptotic Bax. © 2004 Elsevier Ltd. All rights reserved.
Source Title: International Journal of Biochemistry and Cell Biology
URI: http://scholarbank.nus.edu.sg/handle/10635/32001
ISSN: 13572725
DOI: 10.1016/j.biocel.2004.05.018
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