Methylcholanthrene causes increased thymocyte apoptosis

Charles T. Lutz, Garvan Browne, C. Rosemarie Petzold

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


The polycyclic aromatic hydrocarbon (PAH), methylcholanthrene (MCA), is a well studied carcinogen and a teratogen. MCA and other PAH cause immune suppression of B cell and T cell responses in mice and MCA had been reported to induce thymus atrophy. Here we show that MCA treatment causes thymus atrophy in adrenalectomized mice and in C57BL/6 and DBA/2 mice which differ in aryl hydrocarbon receptor (AhR) expression. This indicates that MCA-mediated thymus atrophy is mediated, at least in part, by glucocorticoid hormone receptor- and aryl hydrocarbon receptor-independent mechanisms. Assay of thymocytes, both in situ and ex vivo, demonstrate that MCA induces thymocyte apoptosis. Apoptotic thymocytes can be found within or adjacent to thymic Mφ, suggesting rapid phagocytosis. Mice that are deficient in tumor necrosis factor-α receptor-1 or p53, or that overexpress bcl-2 are susceptible to MCA-mediated thymus atrophy.

Original languageEnglish
Pages (from-to)151-167
Number of pages17
Issue number2
StatePublished - Jul 3 1998

Bibliographical note

Funding Information:
We thank Carol Bray for expert technical assistance and Dr Robert Schelper for helpful discussions. This work was supported by the Roy J. Carver Charitable Trust and by NIH Training Grant T32 AI07260 to Garvan Browne.


  • Apoptosis
  • Methylcholanthrene
  • Ontogeny
  • T-cell
  • Thymus

ASJC Scopus subject areas

  • Toxicology


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