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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jing, Y. Articles by Waxman, S. Search for Related Content PubMed PubMed Citation Articles by Jing, Y. Articles by Waxman, S. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 94 No. 6 (September 15), 1999: pp. 2102-2111 Arsenic Trioxide Selectively Induces Acute Promyelocytic Leukemia Cell Apoptosis Via a Hydrogen Peroxide-Dependent Pathway Yongkui Jing, Jie Dai, Ruth M.E. Chalmers-Redman, Willam G. Tatton, and Samuel Waxman From the Rochelle Belfer Chemotherapy Foundation Laboratory, Division of Neoplastic Diseases, Department of Medicine, and the Department of Neurology, Mount Sinai Medical Center, New York, NY. Low concentrations of As2O3 (1 µmol/L) induce long-lasting remission in patients with acute promyelocytic leukemia (APL) without significant myelosuppressive side effects. Several groups, including ours, have shown that 0.5 to 1 µmol/L As2O3 induces apoptosis in APL-derived NB4 cells, whereas other leukemic cells are resistant to As2O3 or undergo apoptosis only in response to greater than 2 µmol/L As2O3. In this report, we show that the ability of As2O3 to induce apoptosis in leukemic cells is dependent on the activity of the enzymes that regulate cellular H2O2 content. Thus, NB4 cells have relatively low levels of glutathione peroxidase (GPx) and catalase and have a constitutively higher H2O2 content than U937 monocytic leukemia cells. Glutathione-S-transferase  (GST), which is important for cellular efflux of As2O3, is also low in NB4 cells. Moreover, As2O3 further inhibits GPX activity and increases cellular H2O2 content in NB4 but not in U937 cells. Selenite pretreatment of NB4 cells increases the activity of GPX, lowers cellular H2O2 levels, and renders NB4 cells resistant to 1 µmol/L As2O3. In contrast, concentrations of As2O3 that alone are not capable of inducing apoptosis in NB4 cells induce apoptosis in the presence of the GPx inhibitor mercaptosuccinic acid. Similar effects are observed by modulating the activity of catalase with its inhibitor, aminotriazol. More important from a therapeutic point of view, U937 and HL-60 cells, which require high concentrations of As2O3 to undergo apoptosis, become sensitive to low, clinically acceptable concentrations of As2O3 when cotreated with these GPx and catalase inhibitors. The induction of apoptosis by As2O3 involves an early decrease in cellular mitochondrial membrane potential and increase in H2O2 content, followed by cytochrome c release, caspase 3 activation, DNA fragmentation, and the classic morphologic changes of apoptosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. H. HAN, H. J. MOON, B. R. YOU, S. Z. KIM, S. H. KIM, and W. H. PARK The Effect of MAPK Inhibitors on Arsenic Trioxide-treated Calu-6 Lung Cells in Relation to Cell Death, ROS and GSH Levels Anticancer Res, October 1, 2009; 29(10): 3837 - 3844. [Abstract] [Full Text] [PDF] M. Kuroki, Y. Ariumi, M. Ikeda, H. Dansako, T. Wakita, and N. Kato Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress J. Virol., March 1, 2009; 83(5): 2338 - 2348. [Abstract] [Full Text] [PDF] R. R. Rosato, J. A. Almenara, S. C. Maggio, S. Coe, P. 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Kakizuka Tumor Growth Inhibition by Arsenic Trioxide (As2O3) in the Orthotopic Metastasis Model of Androgen-independent Prostate Cancer Cancer Res., July 1, 2001; 61(14): 5432 - 5440. [Abstract] [Full Text] [PDF] O. Sordet, C. Rebe, I. Leroy, J.-M. Bruey, C. Garrido, C. Miguet, G. Lizard, S. Plenchette, L. Corcos, and E. Solary Mitochondria-targeting drugs arsenic trioxide and lonidamine bypass the resistance of TPA-differentiated leukemic cells to apoptosis Blood, June 15, 2001; 97(12): 3931 - 3940. [Abstract] [Full Text] [PDF] S. Waxman and K. C. Anderson History of the Development of Arsenic Derivatives in Cancer Therapy Oncologist, April 1, 2001; 6(90002): 3 - 10. [Abstract] [Full Text] S. L. Soignet Clinical Experience of Arsenic Trioxide in Relapsed Acute Promyelocytic Leukemia Oncologist, April 1, 2001; 6(90002): 11 - 16. [Abstract] [Full Text] Y. Jing, L. Wang, L. Xia, G.-q. Chen, Z. Chen, W. H. Miller, and S. Waxman Combined effect of all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia cells in vitro and in vivo Blood, January 1, 2001; 97(1): 264 - 269. [Abstract] [Full Text] [PDF] R. Uslu, U. A. Sanli, C. Sezgin, B. Karabulut, E. Terzioglu, S. B. Omay, and E. Goker Arsenic Trioxide-mediated Cytotoxicity and Apoptosis in Prostate and Ovarian Carcinoma Cell Lines Clin. Cancer Res., December 1, 2000; 6(12): 4957 - 4964. [Abstract] [Full Text] M. J. McCabe Jr., K. P. Singh, S. A. Reddy, B. Chelladurai, J. G. Pounds, J. J. Reiners Jr., and J. C. States Sensitivity of Myelomonocytic Leukemia Cells to Arsenite-Induced Cell Cycle Disruption, Apoptosis, and Enhanced Differentiation Is Dependent on the Inter-Relationship between Arsenic Concentration, Duration of Treatment, and Cell Cycle Phase J. Pharmacol. Exp. Ther., November 1, 2000; 295(2): 724 - 733. [Abstract] [Full Text] G. J. Roboz, S. Dias, G. Lam, W. J. Lane, S. L. Soignet, R. P. Warrell Jr, and S. Rafii Arsenic trioxide induces dose- and time-dependent apoptosis of endothelium and may exert an antileukemic effect via inhibition of angiogenesis Blood, August 15, 2000; 96(4): 1525 - 1530. [Abstract] [Full Text] [PDF] Y. Huang, C. M. Horvath, and S. Waxman Regrowth of 5-Fluorouracil-treated Human Colon Cancer Cells Is Prevented by the Combination of Interferon {{gamma}}, Indomethacin, and Phenylbutyrate Cancer Res., June 1, 2000; 60(12): 3200 - 3206. [Abstract] [Full Text] S. Zhuang, J. T. Demirs, and I. E. Kochevar p38 Mitogen-activated Protein Kinase Mediates Bid Cleavage, Mitochondrial Dysfunction, and Caspase-3 Activation during Apoptosis Induced by Singlet Oxygen but Not by Hydrogen Peroxide J. Biol. Chem., August 18, 2000; 275(34): 25939 - 25948. [Abstract] [Full Text] [PDF] B. A. Wagner, G. R. Buettner, L. W. Oberley, C. J. Darby, and C. P. Burns Myeloperoxidase Is Involved in H2O2-induced Apoptosis of HL-60 Human Leukemia Cells J. Biol. Chem., July 14, 2000; 275(29): 22461 - 22469. [Abstract] [Full Text] [PDF] Y. Yang, J.-Z. Cheng, S. S. Singhal, M. Saini, U. Pandya, S. Awasthi, and Y. C. Awasthi Role of Glutathione S-Transferases in Protection against Lipid Peroxidation. OVEREXPRESSION OF hGSTA2-2 IN K562 CELLS PROTECTS AGAINST HYDROGEN PEROXIDE-INDUCED APOPTOSIS AND INHIBITS JNK AND CASPASE 3 ACTIVATION J. Biol. Chem., May 25, 2001; 276(22): 19220 - 19230. [Abstract] [Full Text] [PDF] M. Neuss, R. Monticone, M. S. Lundberg, A. T. Chesley, E. Fleck, and M. T. Crow The Apoptotic Regulatory Protein ARC (Apoptosis Repressor with Caspase Recruitment Domain) Prevents Oxidant Stress-mediated Cell Death by Preserving Mitochondrial Function J. Biol. Chem., August 31, 2001; 276(36): 33915 - 33922. [Abstract] [Full Text] [PDF]

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