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RECORD NUMBER: 7 OF 7

OLS Field Name OLS Field Data
Main Title Prophage Induction by DNA Topoisomerase II Poisons and Reactive-Oxygen Species: Role of DNA Breaks.
Author DeMarini, D. M. ; Lawrence, B. K. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Genetic Toxicology Div.
Publisher c1992
Year Published 1992
Report Number EPA/600/J-92/233;
Stock Number PB92-195866
Additional Subjects DNA topoisomerase II ; DNA damage ; Mutagens ; Toxicology ; Phage lambda ; Enzyme inhibitors ; Oxygen ; Free radicals ; SOS response(Genetics) ; Intercalating agents ; Hydrogen peroxide ; Ellipticine ; Doxorubicin ; Paraquat ; DNA gyrase ; Reprints ;
Holdings
Library Call Number Additional Info Location Last
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Status
NTIS  PB92-195866 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 08/22/1992
Collation 19p
Abstract
The following compounds induced prophage lambda in the Escherichia coli WP2(s)Lambda Microscreen assay: adriamycin, m-AMSA, ellipticine, nalidixic acid, oxolinic acid, paraquat, hydrogen peroxide, and sodium azide. Actinomycin D, novobiocin, teniposide, and potassium superoxide did not induce prophage lambda. An inhibitor of DNA gyrase subunit B (novobiocin) does not induce prophage. In contrast, poisons of DNA gyrase subunit A (nalidixic acid and oxolinic acid) were the most potent inducers of prophage among the agents examined here. The next most potent agents were the mammalian DNA topoisomerase II poisons that are reactive intercalators and generators of active-oxygen species (adriamycin and ellipticine). Agents that produce reactive-oxygen species only (hydrogen peroxide and paraquat) were next in potency. The mammalian DNA topoisomerase II poison m-AMSA was the weakest inducer. The results illustrate the relative effectiveness of agents that induce prophage by various mechanisms. Nonetheless, these agents may induce prophage and SOS response by producing essentially the same type of DNA damage, i.e., DNA strand breaks. The study and a review of the literature suggest that certain agents may induce their genotoxic effects in bacteria by mechanisms that are different than those by which they induce their genotoxic effects in mammalian cells.