[The comparison between the mechanisms of sodium selenite induced apoptosis and arsenic trioxide induced apoptosis in human acute promyelocytic leukemia cell line NB4 cells].
In order to explore the differences between the mechanisms of selenite-induced apoptosis and arsenic induced apoptosis in NB4 cells, growth inhibition was determined by MTT test, apoptosis determined by DNA electrophoresis and analysis of intracellular DNA contents, reactive oxygen species and reduced glutathione in the cell were measured by Lucigenin dependent chemoluminescent (CL) test and spectrophotometry, and mitochondrial transmembrane potential was measured by flow cytometry. The results showed that: 5 micro mol/L sodium selenite similar to 1 micro mol/L arsenic trioxide could induce the apoptosis of NB4 cells after treatment for 24 hours. Both could elevate the level of reactive oxygen species and intensify mitochondrial transmembrane potential collapse, accompanied with decrease of reduced glutathione centent. The effect of selenium selenite on these aspects was more significant than those of arsenic trioxide. Elevation of intracellular glutathione in N-acytlcysteine pretreated NB4 cells could enhance the selenite induced apoptosis and oxidative stress, but ameliorate the arsenic trioxide induced apoptosis and oxidative stress. It was concluded that sodium selenite and arsenic trioxide can induce the apoptosis of NB4 cells, but there are significant differences between the mechanisms of selenite-induced and arsenic-induced apoptosis in NB4 cells, particularly in the influence of intracellular glutathione content on the drug action.
Zuo
Lu
L
Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100730, China.
Li
Jian
J
Shen
Ti
T
Zhang
Zhi-Nan
ZN
D000111:Acetylcysteine / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D000077237:Arsenic Trioxide; D001152:Arsenicals / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D004273:DNA, Neoplasm / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D005434:Flow Cytometry; D005978:Glutathione / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007425:Intracellular Membranes / Q000187:drug effects / Q000502:physiology; D015473:Leukemia, Promyelocytic, Acute / Q000378:metabolism* / Q000473:pathology; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology; D010087:Oxides / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D018038:Sodium Selenite / Q000494:pharmacology*; D014407:Tumor Cells, Cultured / Q000187:drug effects
D001152:Arsenicals; D004273:DNA, Neoplasm; D010087:Oxides; D017382:Reactive Oxygen Species; D005978:Glutathione; D018038:Sodium Selenite; D000077237:Arsenic Trioxide; D000111:Acetylcysteine