Metabolic activation of carcinogens in the salmonella mutagenicity assay by hamster and rat liver S‐9 preparations

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Abstract
Before exerting a carcinogenic or mutagenic effect, many carcinogens must undergo metabolic activation. Liver S‐9 preparations from rats treated with Aroclor 1254 (AC) have been widely used to extend the ability of the Salmonella mutagenicity assay to detect such nondirect‐acting agents. We compared the mutagen‐activating capabilities of liver S‐9 preparations from both Syrian golden hamsters and Sprague‐Dawley rats. The comparison was made between S‐9 fractions from untreated, and phenobarbital (PB)‐ and AC‐treated animals of both sexes. Also compared was the effect of varying the amount of S‐9 protein. The preparations from hamster liver were consistently more effective than preparations from rat liver for the activation of 2‐acetylaminofluorene (AAF), 2‐aminoanthracene (AA) (except for AC‐induced preparations), 3‐methylcholanthrene (MCA), and diethylnitrosamine (DEN) to their mutagenic forms. Induced preparations from rats were more active than those from hamsters when using benzo(a)pyrene (BP), while with uninduced preparations, the opposite was true.There was also a relationship between the amount of S‐9 protein and the number of revertant colonies obtained. With the aromatic amines (AAF and AA), a partial inhibition of mutagenicity occurred at the highest protein concentrations tested. With BP, an inverse relationship was observed between protein concentration and the number of revertants occurring in the presence of the preparation from PB‐ and AC‐induced male and female rats.The relative order of activities of aryl hydrocarbon hydroxylase (AHH) and BP‐4,5‐epoxide hydrase (EH) in the preparations was AC‐induced > PB‐.

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