Eliezer Huberman
Oak Ridge National Laboratory
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Cancer Letters | 1979
Thomas J. Slaga; Eliezer Huberman; J. DiGiovanni; G. L. Gleason; Ronald G. Harvey
The skin tumor-initiating and V79 mutagenic activities of various derivatives of 7,12-dimethylbenz[a]anthracene (DMBA) were investigated to determine what possible cellular metabolite(s) may be responsible for its carcinogenicity and/or mutagenicity. 1-,2-,3-,4- and 5-hydroxyDMBA were found to be essentially inactive as skin tumor initiators whereas 9- and 10-hydroxyDMBA had weak activity. The (+/-)-trans DMBA 8,9- and 5,6-dihydrodiols were also essentially inactive as skin tumor initiators and (+/-)-DMBA 8beta,9alpha-diol-10alpha-11alpha-epoxide had weak skin tumor initiating activity. All of the above tested derivatives of DMBA were essentially inactive as mutagens in the cell-mediated or direct V79 mutagenesis systems. A methyl or fluoro addition to the 1, 2 or 5 positions almost completely blocked the skin tumor initiating and V79 mutagenic activities of DMBA, whereas a fluoro addition to position 11 did not. From our data we suggest that a bay region diol-epoxide may be important in DMBA carcinogenicity and mutagenicity.
Cancer Letters | 1978
Eliezer Huberman; Shen K. Yang; David W. McCourt; Harry V. Gelboin
The mutagenicity for mammalian cells of benzo(a)pyrene (BP) and 9 of its derivatives was tested by resistance to ouabain in Chinese hamster V78 cells. The derivatives included the (-) and (+) enantiomers of trans-7,8-diol; the racemic (+/-)trans-7,8-diol; two triols, (7/8,9)-triol and (7,9/8)-triol; and four tetrols, (7,10/8,9)-tetrol, (7/8,9,10)-tetrol, (7,9/8,10-triol and (7,9,10/8)-tetrol. Since V78 cells do not metabolize polycyclic hydrocarbons, mutagenesis was tested both in the presence and in the absence of Golden hamster cells capable of metabolizing polycyclic hydrocarbons. Neither BP nor any of its 9 tested derivatives showed mutagenicity for V78 cells in the absence of normal Golden hamster cells. However, in the presence of these cells, BP and the optically active and racemic trans-7,8-diols exhibited a mutagenic response that was dose-dependent. All other derivatives were inactive. The most active mutagenic hydrocarbon was (-) trans-7,8-diol, and activity decreased in the order (+/-)trans-7,8-diol, (+) trans-7,8-diol and BP.
Basic life sciences | 1983
Carol Jones; Eliezer Huberman
Researchers estimate that environmental chemicals are responsible for a portion of human cancers. These chemicals, identified as potential carcinogens by epidemiology or experimental studies, constitute a very diverse group and thus are likely to interact in the carcinogenic process at different stages and to varying degrees.
Archive | 1978
Eliezer Huberman; Robert Langenbach
Currently there is an increased interest in developing short-term bioassays for carcinogens in view of the studies which implicate a large number of environmental chemicals in causing cancer. While the mechanism by which chemicals induce cancer is unknown, one of the simplest explanations is that carcinogenesis is initiated by a somatic mutation. Indeed, chemical carcinogens are capable of binding to the DNA of susceptible mammalian cells (1–6), and can induce mutations at different genetic loci (25). Some of these mutations could also involve the genes that control the expression of malignant transformation (7–10). Studies of the mutagenic activity of carcinogens in mammalian cells should therefore provide an important technique for detecting cancer-causing agents and possibly for elucidating the mechanism of carcinogenesis (10–15). However, most compounds encountered in the environment are chemically nonreactive and have to be enzymatically activated before they can manifest biological activity (16–17). Furthermore, many mammalian cell lines which are suitable for studies on mutagenesis are not able to metabolically activate these chemicals (18–22).
Proceedings of the National Academy of Sciences of the United States of America | 1981
Eliezer Huberman; Charles Weeks; Adria Herrmann; Michael F. Callaham; Thomas J. Slaga
Cancer Research | 1978
Thomas J. Slaga; Eliezer Huberman; James K. Selkirk; Ronald G. Harvey; W. M. Bracken
Cancer Research | 1979
Eliezer Huberman; Thomas J. Slaga
Cancer Research | 1980
Myles C. Cabot; Clement J. Welsh; Michael F. Callaham; Eliezer Huberman
Carcinogenesis | 1982
Eliezer Huberman; Gary R. Braslawsky; Michael F. Callaham; Hirota Fugiki
Proceedings of the National Academy of Sciences of the United States of America | 1979
Eliezer Huberman; Ming W. Chou; Shen K. Yang