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 Bonin, A. M.
Right arrow Articles by Holder, G. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bonin, A. M.
Right arrow Articles by Holder, G. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1989 Oxford University Press

research-article

The mutagenicity of dibenz[a, j]acridine, some metabolites and other derivatives in bacteria and mammalian cells

Antonio M. Bonin , Christopher A. Rosario 1 2, Colin C. Duke 1, Robert S.U. Baker , Adrian J. Ryan 1 and Gerald M. Holder 1

1The Department of Pharmacy, The University of Sydney Sydney, NSW, 2006, Australia
Toxicology Unit, National Institute of Occupational Health and Safety Sydney, NSW, 2006, Australia

Dibenz[a,j]acridine (DBAJAC) was studied because of its close structural relationship with a number of important carcinogenic polycyclic and azaaromatic hydrocarbons. It was of particular relevance to examine the mutagenicity of known or proposed ‘bay-region’ metabolites, which may be proximate or ultimate carcinogenic derivatives of DBAJAC. Trans-1,2-, 3, 4- and 5, 6-dihydrodiols, the 4- and 6-phenols, the 5, 6-oxide and N-oxide derivatives, and anti- and syn-3, 4-diol 1, 2-epoxides of DBAJAC were examined for their mutagenicity in Salmonella typhimurium TA98 and TA100 and in V79 Chinese hamster lung cells. Of all the compounds studied which require metabolic activation, the 3, 4-dihydrodiol was the most active in both TA100 and in V79 cells. The activity of the 3, 4-dihydrodiol enantiomers was also tested in strain TA100 where no difference was observed from that of the racemic mixture. In V79 cells only the 3R, 4R-dihydrodiol was active, the activity being about three times that of the racemic material. Salmonella strains TA98 and TA100 also differed in their sensitivity towards DBAJAC dihydrodiols, the 1, 2-isomer being of greatest activity in TA98. The most mutagenic compounds in both mammalian and bacterial cells were the ‘bay-region’ diol epoxides of DBAJAC which did not require metabolic activation by S9 mix. The anti-DBAJAC 3, 4-diol 1, 2-epoxide was more mutagenic than the syn form in V79, TA98 and TA100 cells. Overall these results suggest that the in vivo biological activity of DBAJAC metabolites is likely to reflect previous findings with other similar polycyclic aromatic hydrocarbons.


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
 CarcinogenesisHome page
S. Kumar, R. L. Chang, A. W. Wood, J. G. Xie, M. T. Huang, X. X. Cui, P. L. Kole, H. C. Sikka, S. K. Balani, A. H. Conney, et al.
Tumorigenicity of racemic and optically pure bay region diol epoxides and other derivatives of the nitrogen heterocycle dibenz[a,h]acridine on mouse skin
Carcinogenesis, June 1, 2001; 22(6): 951 - 955.
[Abstract] [Full Text] [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.