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Identically, using the lacI mutation detection system, the mutant frequencies were 6.4±3.1×10−5 and 5.8±2.0×10−5.
Mutant frequencies obtained were 10 times higher from the chronic exposure than produced by a nearly lethal acute dose.
In addition, a +1 frameshift mutation, i.e., CCC to CCCC, was introduced in the coding region of the TK1 gene to measure the mutant frequencies.
Doubling time and spontaneous TK mutant frequencies of the established cell lines were similar to those of the wild-type cells.
This indicates that lacZ mutant frequencies are not correlated with a specific DNA repair defect and eventual tumor outcome, at least not in the experimental design presented here.
While liver DNA adduct concentrations were similar in magnitude, mutant frequencies in the DMN-exposed medaka were up to 20 times higher than in the Big Blue rats.
The study did not show any mutation or adduct induction in the exposed group compared to the control group: cII mutant frequencies were 11.0±4.5×10−5 and 11.0±4.8×10−5 in control and exposed lungs, respectively.
An analysis of variance model was fit on the transformed mutant frequencies [11].
Mutant frequencies in these sub-parts also increased significantly with age.
For comparison of mutant frequencies, Fisher's (two-tailed) unpaired exact test was used.
The mean cumulative mutant frequencies obtained for the brain and small intestine were log transformed.
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