The Ah Receptor Is Not Involved in 2,3,7,8-Tetrachlorodibenzo-p-dioxin-mediated Apoptosis in Human Leukemic T Cell Lines

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental pollutant causing public concern. Its toxic effects include disruption of the immune, endocrine, and reproductive systems, impairment of fetal development, carcinogenicity, and lethality in rodents. Here, we report that TCDD induce...

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Bibliographic Details
Published in:The Journal of biological chemistry 1998-07, Vol.273 (31), p.19853-19858
Main Authors: Hossain, Anwar, Tsuchiya, Shigeru, Minegishi, Masayoshi, Osada, Motonobu, Ikawa, Shuntaro, Tezuka, Fumi-aki, Kaji, Mitsuji, Konno, Tasuke, Watanabe, Minro, Kikuchi, Hideaki
Format: Article
Language:English
Subjects:
Apoptosis - drug effects
Aspartic Acid - analogs & derivatives
Aspartic Acid - pharmacology
Benzofurans - pharmacology
beta-Naphthoflavone - pharmacology
Calcium-Calmodulin-Dependent Protein Kinases - metabolism
Cycloheximide - pharmacology
DNA Fragmentation - drug effects
Environmental Pollutants - toxicity
Enzyme Activation - drug effects
Gene Expression Regulation, Neoplastic - drug effects
Genistein - pharmacology
Humans
JNK Mitogen-Activated Protein Kinases
Lymphoma, T-Cell - metabolism
Microscopy, Fluorescence
Mitogen-Activated Protein Kinases
Mutation - genetics
Polychlorinated Dibenzodioxins - toxicity
Proto-Oncogene Proteins c-bcl-2 - metabolism
Receptors, Aryl Hydrocarbon - metabolism
RNA, Messenger - metabolism
Tumor Cells, Cultured
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Summary:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental pollutant causing public concern. Its toxic effects include disruption of the immune, endocrine, and reproductive systems, impairment of fetal development, carcinogenicity, and lethality in rodents. Here, we report that TCDD induces apoptosis in two cultured human leukemic lymphoblastic T cell lines. This cell death was found not to be dependent on an aryl hydrocarbon receptor and to be inhibited by the inhibitor of tyrosine kinases and caspases. Apoptosis-linked c-Jun N-terminal kinase is rapidly activated in these cells by the treatment with TCDD. A dominant-negative mutant of c-Jun N-terminal kinase prevented cell death in the treatment with TCDD. Furthermore, TCDD decreases the Bcl-2 protein level in these cell lines. These findings will help in the understanding of the molecular mechanism underlying TCDD-mediated immunotoxicity.
ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.273.31.19853