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ToxSci Advance Access published online on February 18, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg002
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received September 30, 2002; accepted November 11, 2002
© 2003 Society of Toxicology

Immunotoxicology

TCDD Treatment Eliminates the Long-Term Reconstitution Activity of Hematopoietic Stem Cells

Ruriko Sakai 1, Teruyuki Kajiume 1, Hiroko Inoue 2, Rieko Kanno 2, Masaki Miyazaki 2, Yuichi Ninomiya 2, Masamoto Kanno 2*

1 Department of Immunology, Graduate School of Biomedical Science, Hiroshima University, Minami-ku, Hiroshima 734-8551, Japan; Japanese Society for the Promotion of Science Research Fellowship for Young Scientists; CREST (Core Research for Evolutional Science and Technology) of Japan Science and Technology Corporation, Kawaguchi, Saitama 332-0012, Japan
2 Department of Immunology, Graduate School of Biomedical Science, Hiroshima University, Minami-ku, Hiroshima 734-8551, Japan; CREST (Core Research for Evolutional Science and Technology) of Japan Science and Technology Corporation, Kawaguchi, Saitama 332-0012, Japan

* To whom correspondence should be addressed. E-mail: mkanno{at}hiroshima-u.ac.jp.


  Abstract

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an endocrine disrupting chemical (EDC), can cause carcinogenesis, immunosuppression, and teratogenesis, through a ligand-activated transcription factor, the aryl hydrocarbon receptor (AHR). Despite remarkable recent advances in stem cell biology, the influence of TCDD on hematopoietic stem cells (HSCs), which possess the ability to reconstitute long-term multi-lineage hematopoiesis, has not been well investigated. In this study we examined the influence of TCDD on HSCs enriched for CD34-, c-kit+, Sca-1+, lineage negative (CD34-KSL) cells. The number of the CD34-KSL cells was found to be increased about four fold upon a single oral administration of TCDD (40 µg/kg-body weight). Surprisingly, we found that these TCDD-treated cells almost lost long-term reconstitution activity. This defect was rescued in Ahr-/- mice. These findings suggest that modulation of AHR/ARNT system activity may have an effect on HSC function or survival.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), hematopoietic stem cells (HSCs), CD34-KSL (CD34-, c-kit+, Sca-1+, lineage negative) cells, long-term reconstitution activity, aryl hydrocarbon receptor (AHR). .


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