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PubMed · 9710156

Methylcholanthrene causes increased thymocyte apoptosis.

C T Lutz·G Browne·C R Petzold
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Abstract

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 Mphi, suggesting rapid phagocytosis. Mice that are deficient in tumor necrosis factor-alpha receptor-1 or p53, or that overexpress bcl-2 are susceptible to MCA-mediated thymus atrophy.

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AnimalsApoptosisB-LymphocytesCarcinogensDNAFemaleFlow CytometryGenetic TechniquesMethylcholanthreneMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAMicroscopy, ElectronPhagocytosisReceptors, Aryl HydrocarbonSpecies SpecificityT-LymphocytesThymus GlandComparative StudyJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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C T Lutz, G Browne, C R Petzold. 1998-07-03. Methylcholanthrene causes increased thymocyte apoptosis.. https://doi.org/10.1016/s0300-483x(98)00043-2

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