Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Emerit, I.
Right arrow Articles by Cerutti, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Emerit, I.
Right arrow Articles by Cerutti, P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1983 Oxford University Press

research-article

Clastogenic action of tumor promoter phorbol-12-myristate-13 acetate in mixed human leukocyte cultures

I. Emerit 1 and P. Cerutti 2

1Laboratory of Experimental Cytogenetics, Institut Biomédical des Cordeliers, Université Pierre et Marie Curie 15, Rue de I'Ecole de Médecine, Paris VI, France
2Department of Carcinogenesis, Swiss Institute for Experimental Cancer Research CH-1066 Epalinges s/Lausanne, Switzerland

The tumor promoter phorbol-12-myristate-13-acelate (PMA) induces chromosomal aberrations in mitogen stimulated human lymphocyte cultures containing monocytes, polymorphonuclear cells (PMN) and platelets. Such cultures produce a diffusible clastogenic factor (CF) in response to PMA which causes aberrations in fresh blood cultures which have not been exposed to PMA. We have studied the contribution of monocytes, PMN and platelets to CF formation. ‘Pure’ lymphocyte cultures (containing no platelets and maximally 1% PMN and 2% monocytes) only produced CF when they were in contact with 1 to 1.8 x 106 monocyles attached to plastic during PMA treatment (18.5 ± 5.3% mitosis with aberrations for CF produced in the presence of monocytes relative to 6.0 ± 4% in their absence). They also produced CF of increasing potency upon addition of 0.25 to 5 x 106 PMN (20.5 ± 5.9% mitosis with aberrations for CF produced in the presence of 5 x 106 PMN). Cultures containing 5–10 platelets/lymphocyte also formed CF upon PMA treatment. Cultures of purified monocytes and PMN were capable of producing CF in the absence of lymphocytes. The presence of bovine erythrocyte CuZn superoxide dismutase during PMA treatment decreased the activity of the resulting CF under all conditions. Catalase prevented CF production from PMN. It is concluded that the presence of monocytes, PMN or platelets is a prerequisite for CF formation by PMA. Neoplastic tissue is usually surrounded by inflammatory leukocytes. CF produced by these cells in response to tumor promoters such as PMA may induce chromosomal damage in the neighboring tumor cells.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
I. Emerit, F. Garban, J. Vassy, A. Levy, P. Filipe, and J. Freitas
Superoxide-mediated clastogenesis and anticlastogenic effects of exogenous superoxide dismutase
PNAS, November 12, 1996; 93(23): 12799 - 12804.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
P. Cerutti
Prooxidant states and tumor promotion
Science, January 25, 1985; 227(4685): 375 - 381.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.