Registration Dossier

Administrative data

Endpoint:
in vitro gene mutation study in bacteria
Remarks:
Type of genotoxicity: gene mutation
Type of information:
experimental study
Adequacy of study:
other information
Reliability:
1 (reliable without restriction)

Data source

Reference
Reference Type:
study report
Title:
Unnamed
Year:
1988
Report Date:
1988

Materials and methods

Test guideline
Qualifier:
according to
Guideline:
OECD Guideline 471 (Bacterial Reverse Mutation Assay)
GLP compliance:
yes
Type of assay:
bacterial reverse mutation assay

Test material

Reference
Name:
Unnamed
Type:
Constituent
Details on test material:
Purity > 99%

Method

Target gene:
In the Salmonella typhimurium strains (TA 1535, TA 100, TA 1537, TA 1538, TA 98) the amino acid histidine locus is the target gene.
In the Escherichia coli strain (WP2 uvrA) the amino acid tryptophan locus is the target gene.

Species / strainopen allclose all
Species / strain / cell type:
S. typhimurium TA 1535, TA 1537, TA 98 and TA 100
Species / strain / cell type:
E. coli WP2 uvr A
Metabolic activation:
with and without
Metabolic activation system:
Rat liver S-9 mix from Arochlor 1254 induced rats
Test concentrations with justification for top dose:
0, 0.8, 4, 20, 100, 500, 2500 µg/plate
Controls
Untreated negative controls:
yes

Results and discussion

Test results
Species / strain:
S. typhimurium TA 1535, TA 1537, TA 98 and TA 100
Metabolic activation:
with and without
Genotoxicity:
negative

Applicant's summary and conclusion

Conclusions:
o-Chlorobenzal chloride is not mitagenic in these bacterial test systems either with or without exogenous metabolic activation at the does levels investigated.
Executive summary:

o-Chlorobenzal chloride was tested for mutagenicity with the strains TA 100, TA 1535, TA 1537, TA 1538, TA 98 of Salmonella typhimurium and on Escherichia coli WP2uvrA.

The mutagenicity studies were conducted in the absence and in the presence of a metabolizing system derived from rat liver homogenate. A dose range of 6 different doses from 0.8 µg/plate to 2500 µg/plate was used.

Control plates without mutagen showed that the number of spontaneous revertant colonies was similar to that described in the literature. All positive control compounds gave the expected increase in the number of revertant colonies.

Toxicity: The test compound proved to be toxic to most of the bacterial strains at 100 µg/plate. 2500 µg/plate was chosen as top dose level for the mutagenetic study.

Mutagenicity: In the absence of the metabolic activation system the test compound did not show a dose dependent increase in the number of revertants in any of the bacterial strains. Also in the presence of a metabolic activation system, treatment of the cells with o-chlorobenzal chloride did not result in relevant increases in the number of revertant colonies.

Summarizing, it can be stated that o-chlorobenzal chloride is not mutagenic in these bacterial test system either with or without exogenous metabolic activation at the does levels investigated.