| Abstract |
1,2,5,6,9,10-Hexabromocyclododecane was evaluated for mutagenicity in vitro in the TA98, TA100, and TA1537 strains of Salmonella typhimurium, both in the presence and absence of Arochlor-induced rat liver S-9 metabolic activation. Bacterial cultures without metabolic activation were tested at concentrations of 0.0, 31.5, 100, 315, 1000, or 3000 ug/plate; bacterial cultures with metabolic activation were tested at 0, 3.15, 10, 31.5, 100, 315, 1000, and 3000 ug/plate; the test compound formed a precipitate at concentrations greater than 1000 ug/plate, possibly affecting the accuracy of the test. Some aromatic and olefinic compounds are metabolized to mutagenic epoxides; epoxides can be inactivated by epoxide hydratase or by conjugation to glutathione. A second trial was performed in TA98 with the same concentrations of test compound and with the addition of 1,1,1-trichloropropene 2,3-oxide, an inhibitor of epoxide hydratase and glutathione, to increase the sensitivity of the test towards compounds activated to mutagenic epoxides. The treatment did not increase the frequency of histidine revertants, either with or without metabolic activation, indicating that the test compound was negative for mutagenicity in Salmonella under the conditions of this assay. Positive control treatment with 10 ug/plate benzo(a)pyrene, 10 ug/plate 2-aminoanthracene, or 90 ug/plate 3- methylcholanthrene (without activation) and 1 ug/plate benzo(a)pyrene 4,5-oxide or 10 ug/plate N-methyl-N'-nitro-N- nitrosoguanidine (with activation) produced the expected large increases in the frequency of histidine revertants. |
