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

FEBS Letters

Terrian, David M.¹  Buttke, Thomas M.²  Pardi, Diane³  Dudek, Ronald W.¹  Tebbey, Paul W.²  Folks, Thomas M.³  Sandstrom, Paul A.³ 

[1] Department of Anatomy and Cell Biology, East Carolina University School of Medicine, Greenville, NC 27858, USA;Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, NC 27858, USA;Retrovirus Diseases Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA

关键词: Cell death;    Membrane lipid;    Antioxidant;    Oxygen radical;    Lymphocyte;    BAPTA-AM;    1;    2-bis(O-aminophenoxy)ethane-N;    N;    N′;    N′-tetraacetic acid acetoxymethyl ester;    HPETE;    hydroperoxyeicosatetraenoic;    acid;    HPODE;    hydroperoxydodecadienoic acid;    MTS;    (3-(4;    5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H -tetrazolium;    inner salt);    ROS;    reactive oxygen species;    TNF-α;    tumor necrosis factor-α;   

DOI  :  10.1016/0014-5793(95)00443-D

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown