Abstract

Objective To explore the influence of mitochondrial permeability transition pore opening and cytochrome C(Cyt C) being discharged on the apoptotic mechanism of HL-60 cell induced by desferrioxamine(DFO), so as to provide scientific basis for the clinicians to adopt the strategy of iron deprivation to treat human leukemia. Methods HL-60 cells were co-cultivated with various concentration of DFO for 24-72 hours, then the apoptotic cells and the changes of mitochondrial membrane potential(ΔΨm) were examined by means of flow cytometry(FCM), and Cyt C in cytoplasm was detected by way of celluar immunohistochemistry. Results The cell apoptotic rate assumed rising ten-dency as the highest rate could be up to(44.10±6.31)%, and the effect was of time-and-dose dependence(P<0.01). FCM could detect the ΔΨm declining(P<0.05), and the Cyt C positive cell rate was higher than the controls, the differences were of statistical significance(P<0.05). Conclusions DFO can induce the HL-60 cells apoptosis, and the possible mechanism is that DFO make the mitochondrial permeability transition pore open and get Cyt C discharged from the mitochondria. Key words: Desferrioxamine; HL-60 cell; Apoptosis; Mitochondrion membrane potential; Cytochrome C

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