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Objective To investigate the effects of arsenic trioxide (As2O3) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells.Methods Human multidrug-resistant leukemia cell line K562/ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 cells were determined using flow cytometry.Results Zero point five to 20 μmol/L As2O3 inhibited the proliferation of K562/ADM cells, and K562/ ADM cells were more sensitive to As2O3 than the parental K562 cells. As2O3-induced apoptosis of K562/ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As2O3 significantly inhibited the P-gp expression of K562/ADM cells, and
Objective To investigate the effects of arsenic trioxide (As2O3) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells. Methods Human multidrug-resistant leukemia cell line K562 / ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 Cells were determined using flow cytometry. Results Zero point five to 20 μmol / L As2O3 inhibited the proliferation of K562 / ADM cells, and K562 / ADM cells were more sensitive to As2O3 than the parental K562 cells. As2O3-induced apoptosis of K562 / ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As2O3 significantly inhibited the P-gp expression of K5 62 / ADM cells, and