TPEN Induces Apoptosis Independently of Zinc Chelator Activity in a Model of Acute Lymphoblastic Leukemia and Ex Vivo Acute Leukemia Cells through Oxidative Stress and Mitochondria Caspase-3- and AIF-Dependent Pathways
Figure 3
TPEN induces mitochondrial depolarization, plasma membrane damage, and chromatin fragmentation in Jurkat cells. ((a)–(c)) Jurkat cells (1 × 106 cells/mL) were incubated with TPEN (3 μM) at 37°C for 1, 3, 6, 12, and 24 h. The cells were then used for several assays. (a) Representative histograms showing SubG1 cell population indicative of DNA fragmentation after TPEN treatment, as described in according to Material and Methods section (b) Representative density (dot) plots showing PI/DiOC6(3) percentage of four different cell populations under TPEN treatment, as described in Material and Methods section. (c) Representative density (dot) plots showing annexin V/7-AAD percentage of four different cell populations under TPEN exposure, as described Material and Methods section. Circled number is the mean percentage of three independent experiments. S.D. values were below ±5% (also for Figures 5 and 6) of the mean values and are not shown.
