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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Toxicological information

Specific investigations: other studies

Currently viewing:

Administrative data

Endpoint:
mechanistic studies
Type of information:
experimental study
Adequacy of study:
supporting study
Reliability:
4 (not assignable)
Rationale for reliability incl. deficiencies:
documentation insufficient for assessment

Data source

Reference
Reference Type:
publication
Title:
Unnamed
Year:
1989

Materials and methods

Test guideline
Qualifier:
equivalent or similar to guideline
Guideline:
other: OECD Guideline 471
Deviations:
yes
Remarks:
unsuitable metabolic activation system, unsuitable S. typhimurium strain
GLP compliance:
no
Type of method:
in vitro
Endpoint addressed:
genetic toxicity

Test material

Constituent 1
Chemical structure
Reference substance name:
Sodium azide
EC Number:
247-852-1
EC Name:
Sodium azide
Cas Number:
26628-22-8
Molecular formula:
N3Na
IUPAC Name:
sodium azide

Results and discussion

Applicant's summary and conclusion

Executive summary:

Sodium azide is unique among mutagens. It is highly mutagenic in many plant and bacterial species but marginally mutagenic in mammalian cells. A possible explanation for this difference in mutagenic efficiency may lie in the inability of mammalian cells to convert azide to the putative ultimate mutagen.

Normal human fibroblasts and Chinese hamster cells or cell-free extracts from these cell lines were treated with azide and the sonicates tested for mutagenicity in Salmonella strain TA1530. Without removal of excess sodium azide, the cell homogenates exhibited a clear positive effect, with 2-4 fold increase in mutation rate. After removal of sodium azide by acid treatment, the number of revertants (15-40 per 0.1 mL cell sonicate) was even lower than control values (60-80 per 0.1 mL cell sonicate) and therefore considered negative.

The data suggest that neither cell line was capable of converting sodium azide to a mutagenic intermediate. In addition, both cell lines expressed the enzyme O-acetylserine (thio)-lyase which is responsible for the conversion of Sodium azide to azidoalanine, the putative mutagenic intermediate. Although mammalian cells possess the enzyme responsible for the conversion of sodium azide to azidoalanine, they appear incapable of converting Sodium azide into a mutagenic intermediate in appreciable quantities. Further, the data support the conclusion that sodium azide may be further modified in mammalian cells to an intermediate that is not genotoxic.