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The Salmonella (Ames) mutagenicity assay with metabolic activation was used as a proxy to measure the carcinogenicity of degradation products (Ames et al. 1975).
In our experiments, metabolic activation was clearly not initiated at the antigen receptor.
Methyl eugenol, with or without S9 metabolic activation, was incubated with calf thymus DNA.
The influence of metabolic activation was tested by adding 500 μL of 4% S9 mix to the pre-incubation mixture.
We compared the results with those obtained when fractions of the enzymes participating in metabolic activation was considered.
The transformation assay did not use an exogenous activation system, thus, all chemical responses depended on the inherent target cell metabolic capacity where metabolic activation was required.
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Despite this, many carcinogens which require metabolic activation are very active transplancentally, as the intrinsic susceptibility of rapidly dividing fetal cells compensates effectively for comparatively low tissue levels of reactive metabolites.
We investigated the mutation signature of BaP because it is a model carcinogen and its metabolic activation is well understood [ 30, 31].
The above studies demonstrate that metabolic activation is not registered by labelled glucose to the same extent as DG or FDG, whether using PET, autoradiographic or biochemical methods.
Although this metabolite has potency in inhibiting the P2Y12 receptor equivalent to that of the parent compound, metabolic activation is not a requirement for IPA to occur.
Mutagenic frameshift responses in the presence of metabolic activation were detected at sites 1 (August and September), 2 (August), and 3 (August, September, and October) (Table 2).
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