Tumour cell killing by tumour necrosis factor: inhibition by anaerobic conditions, free-radical scavengers and inhibitors of arachidonate metabolism.

摘要: Previous work on the mechanism of tumour-cell killing by macrophage product tumour necrosis factor (TNF) is consistent with a free radical-induced process. In this study, free-radical involvement was sought (i) investigating effects TNF cytolysis anaerobic conditions, scavengers and inhibitors two potential pathways generation (oxidative phosphorylation arachidonate metabolism) (ii) looking for increased malonyldialdehyde (MDA) production in TNF-treated cells (MDA lipid peroxidation product). Although L929 inhibited only limited were seen scavengers. Suppression metabolism steroids effectively but mitochondrial poison rotenone did not. There marked, late, increase MDA cells. Overall, these results indicate that if radicals are involved it at late stage cytolytic However most striking observation study an essential link