Cytotoxic activity of tumor necrosis factor is inhibited by amiloride derivatives without involvement of the Na+/H+ antiporter

FEBS Letters

Van Roy, F.³  Vanhaesebroeck, B.³  Pouysségur, J.¹  Beyaert, R.³  Fiers, W.³  Cragoe, E.J.² 

[1] Centre de Biochimie, CNRS, Université de Nice, Parc Valrose, 06034 Nice, France;2211 Oak Terrace Drive, Lansdale, PA 19446, USA;Laboratory of Molecular Biology, State University, Gent, Belgium

关键词: Tumor necrosis factor;    Cytotoxicity;    Amiloride;    Na+/H+ antiporter;    Cytokine;    ActD;    aetinomycin D;    CHX;    cycloheximide;    DMA;    5-(N;    N-dimethyl)amiloride;    DMSO;    dimethyl sulfoxide;    EIPA;    5-(N-ethyl-N-isopropyl)amiloride;    HMA;    5-(N;    N-hexamethylene)-amiloride;    MIBA;    5-(N-methyl-N-isobutyl)amiloride;    MGCMA;    5-(N-methyl-N-(guanidinocarbonylmethyl))amiloride;    MTT;    3-(4;    5-dimethylthiazol-2-yl) diphenyltetrazolium bromide;    OD;    optical density;    TNF;    tumor necrosis factor;    U;    units/ml;   

DOI  :  10.1016/0014-5793(90)80581-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Cytotoxicity of tumor necrosis factor (TNF) on L929s cells was efficiently blocked by several amiloride analogs but not by amiloride itself. This protection did not require RNA or protein synthesis. Na⁺/H⁺ antiporter-negative L-M(TK⁻) cells (LAP) could be killed by TNF, showing that the Na⁺/H⁺ exchanger is not required for TNF-cytotoxicity. Similar protection against TNF-mediated cell lysis by amiloride derivatives was found for LAP and L929s cells, excluding a blockade of the Na⁺/H⁺ antiporter as the cause of the protection against TNF by these agents.

【 授权许可】

Unknown