Lipid hydroperoxide-induced apoptosis: lack of inhibition by Bcl-2 over-expression

Paul A. Sandstrom; Diane Pardi; Paul W. Tebbey; Ronald W. Dudek; David M. Terrian; Thomas M. Folks; Thomas M. Buttke

doi:10.1016/0014-5793(95)00443-D

Lipid hydroperoxide-induced apoptosis: lack of inhibition by Bcl-2 over-expression

Paul A. Sandstrom, Diane Pardi, Paul W. Tebbey, Ronald W. Dudek, David M. Terrian, Thomas M. Folks, Thomas M. Buttke

Research output: Contribution to journal › Article › peer-review

107 Scopus citations

Abstract

Increased membrane lipid peroxidation has recently been implicated as being associated with apoptosis. In the present study the addition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE) or 13-hydroperoxydodecadienoic acid (13-HPODE) to A3.01 T cells is shown to induce marked chromatin condensation coincident with DNA fragmentation, indicative of apoptosis. 15-HPETE also evoked an immediate and sustained rise in cytoplasmic calcium which was required for the induction of apoptosis. A3.01 cells transfected with the bcl-2 proto-oncogene were 6- to 8-fold more resistant to apoptotic killing by tumor necrosis factor-α, but only 0.4-fold more resistant to 15-HPETE. Thus, Bcl-2 is not capable of protecting cells from undergoing apoptosis following the direct addition of lipid hydroperoxides.

Original language	English (US)
Pages (from-to)	66-70
Number of pages	5
Journal	FEBS Letters
Volume	365
Issue number	1
DOIs	https://doi.org/10.1016/0014-5793(95)00443-D
State	Published - May 22 1995

Keywords

Antioxidant
Cell death
Lymphocyte
Membrane lipid
Oxygen radical

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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@article{650597eeeda4496a91dd02a68b8e99da,

title = "Lipid hydroperoxide-induced apoptosis: lack of inhibition by Bcl-2 over-expression",

abstract = "Increased membrane lipid peroxidation has recently been implicated as being associated with apoptosis. In the present study the addition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE) or 13-hydroperoxydodecadienoic acid (13-HPODE) to A3.01 T cells is shown to induce marked chromatin condensation coincident with DNA fragmentation, indicative of apoptosis. 15-HPETE also evoked an immediate and sustained rise in cytoplasmic calcium which was required for the induction of apoptosis. A3.01 cells transfected with the bcl-2 proto-oncogene were 6- to 8-fold more resistant to apoptotic killing by tumor necrosis factor-α, but only 0.4-fold more resistant to 15-HPETE. Thus, Bcl-2 is not capable of protecting cells from undergoing apoptosis following the direct addition of lipid hydroperoxides.",

keywords = "Antioxidant, Cell death, Lymphocyte, Membrane lipid, Oxygen radical",

author = "Sandstrom, {Paul A.} and Diane Pardi and Tebbey, {Paul W.} and Dudek, {Ronald W.} and Terrian, {David M.} and Folks, {Thomas M.} and Buttke, {Thomas M.}",

year = "1995",

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doi = "10.1016/0014-5793(95)00443-D",

language = "English (US)",

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T1 - Lipid hydroperoxide-induced apoptosis

T2 - lack of inhibition by Bcl-2 over-expression

AU - Sandstrom, Paul A.

AU - Pardi, Diane

AU - Tebbey, Paul W.

AU - Dudek, Ronald W.

AU - Terrian, David M.

AU - Folks, Thomas M.

AU - Buttke, Thomas M.

PY - 1995/5/22

Y1 - 1995/5/22

N2 - Increased membrane lipid peroxidation has recently been implicated as being associated with apoptosis. In the present study the addition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE) or 13-hydroperoxydodecadienoic acid (13-HPODE) to A3.01 T cells is shown to induce marked chromatin condensation coincident with DNA fragmentation, indicative of apoptosis. 15-HPETE also evoked an immediate and sustained rise in cytoplasmic calcium which was required for the induction of apoptosis. A3.01 cells transfected with the bcl-2 proto-oncogene were 6- to 8-fold more resistant to apoptotic killing by tumor necrosis factor-α, but only 0.4-fold more resistant to 15-HPETE. Thus, Bcl-2 is not capable of protecting cells from undergoing apoptosis following the direct addition of lipid hydroperoxides.

AB - Increased membrane lipid peroxidation has recently been implicated as being associated with apoptosis. In the present study the addition of 15-hydroperoxyeicosatetraenoic acid (15-HPETE) or 13-hydroperoxydodecadienoic acid (13-HPODE) to A3.01 T cells is shown to induce marked chromatin condensation coincident with DNA fragmentation, indicative of apoptosis. 15-HPETE also evoked an immediate and sustained rise in cytoplasmic calcium which was required for the induction of apoptosis. A3.01 cells transfected with the bcl-2 proto-oncogene were 6- to 8-fold more resistant to apoptotic killing by tumor necrosis factor-α, but only 0.4-fold more resistant to 15-HPETE. Thus, Bcl-2 is not capable of protecting cells from undergoing apoptosis following the direct addition of lipid hydroperoxides.

KW - Antioxidant

KW - Cell death

KW - Lymphocyte

KW - Membrane lipid

KW - Oxygen radical

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