Suppression of mitochondrial respiration and increased glycolysis are charaeteristic features of activated macrophages. We show here that antimycin A, a respiratory inhibiter,inducedinterleukin-1syRthesisandtumericidalactivity without inducing tumer necresis factor er nitric oxide. The induction of tumoricidal actiyity was resista!it te inhibitors of tyrosine-specific protein kinases and intracellular glycoprotein transport. The cognate interaction between macrophages and target cells was not a prerequisite fer the tumericidal activity. In contrast, lipopolysaccharide induced the production of interleukin-1, tumor ilecrosis factor and nitric oxide, the induction of tumoricida} actiyity being sensitive to genistein and brefeldin A. Antimycin A, like lipopolysaccharide, induced the Telease of a cytoplasmic enzyme and apoptosis ef macrophages. Antimycin A showed anti-metastatic activity in vivo. These results suggest that the inhibition of oxidative respiration would induce apoptosis and the resultant release ef soluble effector molecules of macrophages whieh inhibit tumor metastasis in vivo,
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