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PubMed1984

Azoreductase activity of Sprague Dawley and Wistar-derived rats towards both carcinogenic and non-carcinogenic analogues of 4-dimethylaminophenylazobenzene (DAB).

Azoreductase activity towards the hepatocarcinogen p-dimethylaminophenylazobenzene (DAB) and four analogues has been measured in vitro in the liver and caecum of Sprague Dawley (Alpk/SD) and Alderley Park (Alpk/AP Wistar-derived) rats. Two carcinogenic DAB analogues, 3'-methyl-p-dimethylaminophenylazobenzene (3M) and 6-p-dimethylaminophenylazobenzothiazole (6BT) and two non-carcinogenic analogues, 4-N-pyrrolidinylazobenzene (4N) and 5-p-dimethylaminophenylazoindazole (5I) have been examined. The azoreductase activity towards DAB of a 9000 g supernatant of liver homogenate was greater in the SD than the AP strain between 6 and 13 weeks of age, but comparable to that of AP rats at 4 weeks of age. The activity towards DAB fell in both strains with increasing age. Animals of both strains fed a riboflavin-low diet (2-3 mg kg-1) had reduced azoreductase activity with DAB when compared to a standard diet at all ages studied, although the difference was less marked in the AP rats. 3M and 4N were azoreduced by the livers of both strains of rat fed a standard diet at a rate of approximately 50% of that of DAB, whereas 5I and 6BT were cleaved at a much lower rate (5-20%). All the chemicals were reduced by an oxygen-insensitive enzyme in the liver preparation, as has previously been reported for DAB. DAB, 3M and 6BT were reduced at a similar rate to each other by a fraction containing caecal contents, both in and between the two strains of rat. Similarly, 4N and 5I were reduced by a caecal preparation at a similar rate to each other in and between both strains of rat, but at a rate of only 30-50% that shown by DAB, 3M and 6BT. In contrast to the conditions required by the liver azoreductase enzyme, anaerobic conditions were required for maximal activity of the caecal preparation. Liver azoreductase activity towards all the DAB analogues was reduced in both strains of rat maintained on a riboflavin-low diet, while the caecal azoreductase activity was unaffected. Neither the activity profile observed in vitro in the liver nor the caecum was found to correlate with the relative carcinogenicity reported for these compounds, suggesting that other factors are more important in determining this toxicity for the series of azo chemicals examined in this study.

Age Factors↗
PubMed1962

Effect of azo dyes on growth and metabolism of Neurospora crassa. I. Relative resistance of Neurospora strains to azo dye inhibition.

Bobb, Dolores (Palo Alto Medical Research Foundation, Palo Alto, Calif.), Dorothy Liebes, and David A. Salzberg. Effect of azo dyes on growth and metabolism of Neurospora crassa. I. Relative resistance of Neurospora strains to azo dye inhibition. J. Bacteriol. 84:242-249. 1962.-Under conditions where growth factors were not limiting, 3'-methyl-4-monoaminoazobenzene, a rat hepatocarcinogen, inhibited growth of six Neurospora strains studied. The strains could be divided into three groups with regard to sensitivity. A wild-type and a leucine-requiring mutant were the most resistant, and the riboflavine-deficient strain, 51602, showed greatest susceptibility. Results suggested a possible correlation between the inhibition of strain 51602 and the ability of the mutant to synthesize riboflavine from its precursors. Inhibition was not dependent on the utilization of externally supplied riboflavine. The azo dye inhibition of all strains resulted primarily in a prolonged lag phase, although growth rates were affected to some degree. Spore germination did not appear to be retarded. A dose-response curve was developed to measure quantitatively the growth inhibition by azo dyes; it was based on the time required for inhibited and control cultures to reach identical growth weights.

Animals↗
PubMed1979

Selection of carcinogens and related compounds tested for mutagenic activity.

A list of 102 chemicals was prepared for subsequent mutagenesis assays in a National Cancer Institute program to determine the extent of correlation between carcinogenesis and mutagenesis in standardized assays. The chemicals were divided into five major categories: 37 aromatic amines, 11 polycyclic aromatic hydrocarbons, 8 nitrosamines and nitrosamides, 16 alkylating agents, and a miscellaneous category consisting of 11 heterocyclic compounds, 7 amides, ureas and acylating agents, 5 antimetabolites, 4 inorganic chemicals, and 3 promoters. The chemicals were further described as procarcinogens (requiring metabolic activation to exert their biologic activities), ultimate carcinogens (direct-acting chemicals not requiring metabolic activation), and noncarcinogens (compounds shown to be inactive in one or more adequate carcinogenicity tests). An extensive bibliography documents the selection and categorization of the compounds.

Alkylating Agents↗