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The role of mitochondrial targeting in arsenic trioxide‐induced apoptosis in myeloid cell lines

Data regarding the role of mitochondria in arsenic trioxide (As2O3)‐induced apoptosis are controversial. We investigated the contribution of caspases and mitochondrial depolarization to As2O3‐induced apoptosis in the myeloid cell lines NB‐4, HL‐60 and U‐937. Caspase inhibition reduced the amount of cells with As2O3 (20 μmol/l)‐induced mitochondrial depolarization by about 50% in all cell lines. As2O3 also induced dose‐dependent phosphatidylserine exposure in cells without depolarized mitochondria. We conclude that caspase activation is of similar importance in As2O3‐induced apoptosis in myeloid cell lines as direct mitochondrial targeting and mitochondria are not necessary for caspase activation downstream of mitochondria.