JPET Introducing ALZET?ew Model 2006 Pump

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Comment, C. E.
Right arrow Articles by Luster, M. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Comment, C. E.
Right arrow Articles by Luster, M. I.

Thymocyte injury after in vitro chemical exposure: potential mechanisms for thymic atrophy

CE Comment, BL Blaylock, DR Germolec, PL Pollock, Y Kouchi, HW Brown, GJ Rosenthal and MI Luster

Systems Toxicity Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.

In addition to hepatic injury, thymic atrophy is a common observation in rodent subchronic toxicity studies. We have examined representative chemicals which produce thymic atrophy in rodents for their ability to cause direct thymocyte injury because the mechanism(s) responsible for these effects have not been determined. Although a number of the compounds examined failed to have any observable direct effect on thymocytes, others either inhibited lymphocyte proliferation or initiated cell death. In the latter group, thymocyte death was always preceded by increases in intracellular Ca++ and involved, to varying degrees, necrotic and apoptotic events. Apoptosis, as evidenced by cellular DNA cleavage into multiples of 180-200-base pair oligonucleotides and partial cell protection by cycloheximide treatment, was most evident after treatment with acetaldehyde or dibutyltin dichloride. A number of compounds that produce thymic atrophy also inhibited T lymphocyte proliferation without evidence of cell death. Considering that many of the compounds tested failed to produce any evidence of direct thymocyte injury (i.e., necrosis, apoptosis or inhibition of cell proliferation), indirect mechanisms may also be involved in thymic atrophy and may target prothymocytes in the bone marrow, after normal homing patterns or injure the thymic epithelium. Thus, it appears that a variety of mechanisms may be responsible for chemical-induced thymic atrophy and/or injury.

Volume 262, Issue 3, pp. 1267-1273, 09/01/1992
Copyright © 1992 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 Mol. Pharmacol.Home page
K.-T. Park, K. A. Mitchell, G. Huang, and C. J. Elferink
The Aryl Hydrocarbon Receptor Predisposes Hepatocytes to Fas-Mediated Apoptosis
Mol. Pharmacol., March 1, 2005; 67(3): 612 - 622.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
Y. Tan, D. Li, R. Song, D. Lawrence, and D. O. Carpenter
Ortho-Substituted PCBs Kill Thymocytes
Toxicol. Sci., December 1, 2003; 76(2): 328 - 337.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1992 by the American Society for Pharmacology and Experimental Therapeutics.