This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Huberman, E. Articles by Sims, P. Search for Related Content PubMed PubMed Citation Articles by Huberman, E. Articles by Sims, P.

Transformation of Hamster Embryo Cells by Epoxides and Other Derivatives of Polycyclic Hydrocarbons¹

McArdle Laboratory for Cancer Research, University of Wisconsin, Madison, Wisconsin 53706 [E. H., T. K., H. M., J. K. S., C. H.], and Chester Beatty Research Institute, London, England [P. L. G., P. S.]

K-region epoxides of dibenz(a,h)anthracene and benz(a)anthracene were more active in producing malignant transformation of hamster embryo cells than the corresponding hydrocarbons, K-regions cis- and trans-dihydrodiols and phenols. The cytotoxicity exerted by epoxides, relative to the other derivatives, varied among those tested. The 8,9-epoxide (non-K-region) of benz(a)anthracene was less active in producing transformation and cytotoxicity than the corresponding 5,6-epoxide (K-region). Expoxides of the K-regions of 3-methylcholanthrene, phenanthrene, and chrysene were also more active in producing cytotoxicity and transformation than the corresponding hydrocarbon. These data support the suggestion that the metabolic production of epoxides of these polycyclic hydrocarbons is a prerequisite for biological activity and that transformation by epoxides is not based on the selection of preexisting transformed cells. The K-region epoxide of 7-methylbenz(a)anthracene was slightly more active than 7-methylbenz(a)anthracene in producing transformation in a 4-hr treatment, but the converse was true with a 7-day exposure. Under both conditions, the activities of 7-bromomethyl-12-methylbenz(a)anthracene and 7-bromomethylbenz(a)anthracene were approximately the same as those of their parent hydrocarbons at producing transformation.

¹ Aided in part by Grant CA-07175 from The National Cancer Institute, NIH, and by Grant E-556 from The American Cancer Society.

² Holder of a Cancer Research Fellowship from the WHO International Agency for Research on Cancer. Present address: Department of Genetics, The Weizmann Institute, Rehovoth, Israel.

³ Holder of NIH International Postdoctoral Fellowship F 05-TW-1541. Present address: Department of Cancer Cell Research, Institute of Medical Science, University of Tokyo, Tokyo, Japan.

⁴ Present address: Sloan-Kettering Institute for Cancer Research, New York, N. Y.

⁵ American Cancer Society Professor of Oncology, to whom requests for reprints should be sent.

⁶ Holder of a Travel Fellowship from WHO International Agency for Research on Cancer.

Received 2/15/72. Accepted 3/23/72.

This article has been cited by other articles:

				F. L. Martin Genotoxins and the initiation of sporadic breast cancer Mutagenesis, March 1, 2001; 16(2): 155 - 161. [Abstract] [Full Text] [PDF]

				D. M. Jerina and J. W. Daly Arene Oxides: A New Aspect of Drug Metabolism Science, August 16, 1974; 185(4151): 573 - 582. [PDF]