Introduction] 1 '-Acetoxychavicol acetate (ACA), obtained from rhizomes of commonly used ethno-medicinal plant Languas galanga (Zingiberaceae) used in southeast Asian countries, showed a potent inhibition towards tumor promoter induced Epstein-Barr virus activation. We sought to evaluate whether ACA exerts its antitumor affects by inducing apoptosis in Ehrlich ascites tumor cells, and further, the mediation of polyamines in the apoptotic events, as determined by morphological changes and caspase-3-like protease activity. pesults] ACA treatment resulted in changes in morphology and a dose-dependent suppression of cell viability. Apoptosis, characterized by nuclear condensation, membrane blebbing and cell shrinkage, and a significant induction of caspase-3-like protease activity at 8 h in a time-course study were observed. Apoptotic bodies formation was preceded by depletion of intracellular polyamines, and both dose and time-dependent inhibitory and activation effect by ACA on ornithine decarboxylase and spermidine/spermine N1acetyltransferase, respectively. Exogenous polyamines administration prevented ACA-induced apoptosis represented by lower apoptotic bodies count, and also caused reduction in the induced caspase-3-like protease activity at 8 h.[Conclusion] These findings suggest the anticarcinogenic effect of ACA might be partly due to depletion of polyamine levels and a triggering of caspase-3-like protease activity that result in apoptosis. Seoul 11 0-799, KoreaThis study investigates the involvement of N-alpha-tosyl -L-phenylalanine chloromethyl ketone (TPCK)-sensitive enzymes in various forms of cell death. The effect of TPCK was studied on both necrotic and apoptotic death processes. TPCK exerted a dual effect on cell death in the human monocytic cell line U937: it has some proapoptotic activity as indicated by changes in membrane potential and cytochrome C release and also protects the cells from undergoing apoptosis and necrosis. TPCK inhibited apoptosis and necrosis induced by anti-Fas, staurosporine and Ca *+ ionophore in the U-937 monocytic cell line.Necrosis was induced in the presence of oligomycin in a glucosefree medium. Similar results were obtained with the Jurkat T-cell line which revealed different sensitivity to necrosis inducers. In order to understand the mode of action of the inhibitor, its effect on mitochondria1 potential was studied. Necrosis and apoptosis induced by anti-Fas were accompanied by a decrease in mitochondria] membrane potential. In both cases, TPCK inhibited this change that occurred prior to other manifestations of cell death. These results suggest that a TPCK-sensitive enzyme is involved in early stages of the death process in addition to the role of these enzymes at the nuclear stage. In summary, our results indicate that TPCK-sensitive proteases play a role at different stages in the overall regulation of cell death processes.

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