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Lipid hydroperoxide‐induced apoptosis: lack of inhibition by Bcl‐2 over‐expression
Author(s) -
Sandstrom Paul A.,
Pardi Diane,
Tebbey Paul W.,
Dudek Ronald W.,
Terrian David M.,
Folks Thomas M.,
Buttke Thomas M.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00443-d
Subject(s) - apoptosis , chemistry , microbiology and biotechnology , biochemistry , biology
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.