The Ah receptor is not involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin- mediated apoptosis in human leukemic T cell lines

Anwar Hossain, Shigeru Tsuchiya, Masayoshi Minegishi, Motonobu Osada, Shuntaro Ikawa, Fumi Aki Tezuka, Mitsuji Kaji, Tasuke Konno, Minro Watanabe, Hideaki Kikuchi

Research output: Contribution to journalArticlepeer-review

63 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)19853-19858
Number of pages6
JournalJournal of Biological Chemistry
Volume273
Issue number31
DOIs
Publication statusPublished - 1998 Jul 31

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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