par Hepburn, Anne ;Boeynaems, Jean-Marie ;Fiers, Walter;Dumont, Jacques Emile
Référence Biochemical and biophysical research communications, 149, 2, page (815-822)
Publication Publié, 1987-12
Référence Biochemical and biophysical research communications, 149, 2, page (815-822)
Publication Publié, 1987-12
Article révisé par les pairs
Résumé : | L929 cells were incubated with tumor necrosis factor-alpha (TNF-alpha) in the presence or absence of various inhibitors of arachidonic acid metabolism. The addition of either hydrocortisone or nordihydroguaiaretic acid (NDGA) decreased the cytotoxic effect of TNF-alpha but exogenously added arachidonate or linoleate, indomethacin and eicosatetraynoic acid (ETYA) were without effect. While it was found that TNF-alpha stimulated arachidonic acid release, no metabolites of this fatty acid could be evidenced. Cytotoxicity of TNF-alpha could also be decreased by the addition of either cholera or pertussis toxin. These results suggest that a GTP-binding protein is involved in the cytotoxic action of TNF-alpha. Arachidonic acid, released possibly by a phospholipase A2, might also play a role, but probably not via its conversion to known metabolites. |