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 journalArticlepeer-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 languageEnglish (US)
    Pages (from-to)66-70
    Number of pages5
    JournalFEBS Letters
    Volume365
    Issue number1
    DOIs
    StatePublished - 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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