X Huang1. 1. Institute of Hematology, Peoples' Hospital, Beijing Medical University, Beijing 100044.
Abstract
OBJECTIVE: To explore the relationship among intercellular -SH, caspase, retinoic acid (RA) and arsenic trioxide(As2O3)-induced apoptosis. METHODS: The in vitro effect of different thiols compounds, RA and caspase inhibitors on As2O3-induced apoptosis in NB4 and HL-60 cells was studied. RESULTS: 1. NAC completely blocked, BSO potentiated while MTG, BAL had no effect on As2O3-induced apoptosis. 2. Z-VAD.fmk blocked while Y-VAD.fmk had no effect on As2O3-induced apoptosis. 3. RA and As2O3 showed synergism in HL-60 cells, while showed antagonism in NB4 cell. CONCLUSIONS: 1. As2O3 binds with intracellular -SH, changes signal transduction, selectively activates caspase and causes apoptosis. 2. The regulating effect of RA on As2O3-induced apoptosis depends on cell types.
OBJECTIVE: To explore the relationship among intercellular -SH, caspase, retinoic acid (RA) and arsenic trioxide(As2O3)-induced apoptosis. METHODS: The in vitro effect of different thiols compounds, RA and caspase inhibitors on As2O3-induced apoptosis in NB4 and HL-60 cells was studied. RESULTS: 1. NAC completely blocked, BSO potentiated while MTG, BAL had no effect on As2O3-induced apoptosis. 2. Z-VAD.fmk blocked while Y-VAD.fmk had no effect on As2O3-induced apoptosis. 3. RA and As2O3 showed synergism in HL-60 cells, while showed antagonism in NB4 cell. CONCLUSIONS: 1. As2O3 binds with intracellular -SH, changes signal transduction, selectively activates caspase and causes apoptosis. 2. The regulating effect of RA on As2O3-induced apoptosis depends on cell types.