Diethyldithiocarbamate-Induced Cytotoxicity and Apoptosis in Leukemia Cell Lines
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概要
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Diethyldithiocarbamate (DDTC) has been shown to induce cytotoxicity in several different systems. We examined whether the DDTC-induced cytotoxicity was via apoptosis, or in relation to intracellular glutathione (GSH) in various murine and human leukemia cell lines. The cells most sensitive to DDTC-induced cytotoxicity were P388 lymphoid neoplasma cells and NALM-6, a B cell line of acute lymphocytic leukemia (ALL). The next level of susceptible cells included J774.1, having a macrophage function, HL-60 premyelocytic leukemia cells, MOLT-4, an acute lymphoblastic leukemia cell, and Jurkat, a T-cell leukemia. U937 (expressing many monocytelike characteristics), K562 erythroleukemia and K562/DXR (a multidrug-resistant clone derived from K562) were almost unaffected by DDTC. P388 was also highly susceptible to H_2O_2, a most useful exogenous reactive oxygen species generator, and was lower in intracellular total GSH content than other leukemia cells. DDTC-induced cytotoxicity was closely related to intracellular GSH, but the level of cellular GSH did not always correlate with H_2O_2-induced cytotoxicity in this experiment. K562 had a higher intracellular total GSH content and showed lower susceptibility to DDTC andH_2O_2 , but with the combination of DDTC and DL-buthionine-(S,R)-sulfoximine (BSO), cytotoxicity increased significantly. The ratio of GSH/GSSG in P388 was reduced by DDTC or H_2O_2. H_2O_2-induced cytotoxicity was completely blocked by catalase (CAT), while it was enhanced by superoxide dismutase (SOD). CAT or SOD did not affect DDTC-induced cytotoxicity. N-Acetylcysteine (NAC: 1 mM), a vanguard substance of GSH, and aurintricarboxylic acid (ATA: 100μM), an endonuclease inhibitor, ameliorated DDTC-induced cytotoxicity and apoptosis. In conclusion, we suggest that DDTC-induced cytotoxicity was via an oxidative shift in the intracellular redox state, and accompanied the activation of endonuclease through apoptosis in leukemia cell lines.
- 公益社団法人日本薬学会の論文
- 2003-07-01
著者
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ISHIKAWA Masaaki
Department of Pharmacology and Toxicology, Cancer Research Institute, Tohoku Pharmaceutical Universi
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KANNO Syu-ichi
Department of Clinical Pharmacotherapeutics, Tohoku Pharmaceutical University
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Kanno Syu-ichi
Department Of Clinical Pharmacotherapeutics Tohoku Pharmaceutical University
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Kanno Syu-ichi
東北薬科大学癌研究所
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Kanno Syu-ichi
東北薬科大学 薬物治療学教室
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Kanno Syu-ichi
Department Of Pharmacology And Toxicology Cancer Research Institute Tohoku Pharmaceutical University
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SHOUJI Ai
Department of Clinical Pharmacotherapeutics, Tohoku Pharmaceutical University
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ASOU Keiko
Department of Pharmacology and Toxicology. Cancer Research Institute, Tohoku Pharmaceutical Universi
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MATSUKAWA Emi
Department of Pharmacology and Toxicology, Cancer Research Institute, Tohoku Pharmaceutical Universi
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MIURA Ai
Department of Pharmacology and Toxicology, Cancer Research Institute, Tohoku Pharmaceutical Universi
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Matsukawa Emi
Department Of Pharmacology And Toxicology Cancer Research Institute Tohoku Pharmaceutical University
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Ishikawa Masaaki
Department Of Clinical Pharmacotherapeutics Tohoku Pharmaceutical University
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Ishikawa Masaaki
Department Of Pharmacology And Toxicology Cancer Research Institute Tohoku Pharmaceutical University
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Ishikawa Masaaki
Department Of Pharmacology And Toxicology Cancer Research Institute Tohoku College Of Pharmacy
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Miura A
Department Of Pharmacology And Toxicology Cancer Research Institute Tohoku Pharmaceutical University
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Shouji Ai
Department Of Clinical Pharmacotherapeutics Tohoku Pharmaceutical University
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Asou Keiko
Department Of Pharmacology And Toxicology. Cancer Research Institute Tohoku Pharmaceutical Universit
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Ishikawa Masaaki
Dep. Of Clinical Pharmacotheraputics Tohoku Pharmaceutical Univ. Jpn
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Miura Ai
Department Of Marine Science And Resources College Of Bioresource Sciences Nihon University
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