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J Biol Chem, Vol. 273, Issue 31, 19853-19858, July 31, 1998
From the Departments of 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.
The Ah Receptor Is Not Involved in
2,3,7,8-Tetrachlorodibenzo- p-dioxin-mediated Apoptosis
in Human Leukemic T Cell Lines
,,,
,, and
Molecular Genetics,
§ Pediatric Oncology, and Pathology,
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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