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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Endpoint:
in vitro gene mutation study in bacteria
Remarks:
Type of genotoxicity: gene mutation
Type of information:
experimental study
Adequacy of study:
key study
Reliability:
1 (reliable without restriction)
Rationale for reliability incl. deficiencies:
other: study performed according to OECD and GLP guidelines
Cross-reference
Reason / purpose for cross-reference:
reference to same study

Data source

Reference
Reference Type:
study report
Title:
Unnamed
Year:
1996
Report date:
1996

Materials and methods

Test guideline
Qualifier:
equivalent or similar to guideline
Guideline:
OECD Guideline 471 (Bacterial Reverse Mutation Assay)
Deviations:
no
GLP compliance:
yes (incl. QA statement)
Type of assay:
bacterial reverse mutation assay

Test material

Constituent 1
Chemical structure
Reference substance name:
6,10-dimethylundeca-5,9-dien-2-one
EC Number:
211-711-2
EC Name:
6,10-dimethylundeca-5,9-dien-2-one
Cas Number:
689-67-8
Molecular formula:
C13H22O
IUPAC Name:
6,10-dimethylundeca-5,9-dien-2-one

Method

Target gene:
TA97a: hisD6610, TA 98: hisD3052; TA 100 and TA 1535 hisG46, TA102: hisG428
Species / strain
Species / strain / cell type:
other: TA1535, TA97, TA98, TA100, and TA102
Additional strain / cell type characteristics:
acetyltransferase deficient
Metabolic activation:
with and without
Metabolic activation system:
S9
Test concentrations with justification for top dose:
0, 1.6, 5, 16.6, 50, 166 ug/plate
Controls
Untreated negative controls:
yes
Negative solvent / vehicle controls:
yes
Positive controls:
yes
Positive control substance:
2-nitrofluorene
sodium azide
mitomycin C
other: 2-aminoanthracene

Results and discussion

Test results
Species / strain:
S. typhimurium, other: TA1535, TA97, TA98, TA100, and TA102
Metabolic activation:
with and without
Genotoxicity:
negative
Untreated negative controls validity:
valid
Positive controls validity:
valid
Remarks on result:
other: all strains/cell types tested
Remarks:
Migrated from field 'Test system'.

Any other information on results incl. tables

-

Applicant's summary and conclusion

Conclusions:
Interpretation of results (migrated information):
negative

Neither Geranylaceton per se, nor any of its metabolites formed under the experimental conditions, induced genetic damage in
the Ames test.
Executive summary:

Geranylaceton was evaluated for mutagenic activity in the Ames test. A standard plate incorporation and a preincubation modification assay in absence and in presence of an exogenous metabolic activation system (S9) were performed. Five

Salmonella typhimurium tester strains (TA1535, TA97, TA98, TA100, and TA102) were

employed. The activity of the S9-mix and the responsiveness of the tester strains were

verified by including appropriate controls into each experiment. Geranylaceton was dissolved in dimethylsulfoxide (DMSO). Toxic effects were observed in a preliminary toxicity experiment, starting at 158 ug/plate (slightly reduced background growth). Therefore concentrations ranging from 1.6 to 166 ug/plate were evaluated in the main experiments. Upon addition to the aqueous

medium, a slight milky suspension was observed at 50 ug/plate (preincubation assay) and 166 ug/plate (both methods). Strain dependent toxicity (reduction in the background growth and/or reduction in the number of revertant colonies) was observed

in the selected concentration range. The toxic effects were more pronounced in absence of an exogenous metabolic activation system and in the experiment using the preincubation method, known to be more sensitive for several class of compounds.

Geranylaceton did not cause a mutagenic effect in any of the five investigated strains.

Thus it can be concluded, that neither Geranylaceton per se, nor any of its metabolites formed under the experimental conditions, induced genetic damage in the Ames test.