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EC number: 203-479-6 | CAS number: 107-29-9
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vivo
Link to relevant study records
- Endpoint:
- in vivo mammalian germ cell study: gene mutation
- Remarks:
- Type of genotoxicity: gene mutation
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Study period:
- 1981
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Well documented study.
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 477 (Genetic Toxicology: Sex-linked Recessive Lethal Test in Drosophila melanogaster)
- GLP compliance:
- not specified
- Type of assay:
- Drosophila SLRL assay
- Species:
- Drosophila melanogaster
- Strain:
- other: Canton-S
- Sex:
- male
- Route of administration:
- oral: feed
- Details on exposure:
- Young adult Canton-S males (post-meiotic germ cell stages) and young adult Canton-S males of 1-2 days old (pre-meiotic germ cell stages) were exposed to 2000 ppm AAO by feeding on glass fiber filter paper that had been inundated with either the exposure or control solution. This method also results in contact exposure and inhalation of any fumes that are present. The solvent used is a 5% sucrose solution kept at a pH of 6.8 by a phosphate buffer (1:1 ratio of 4.539 g KH2PO4 per L and 5.938g Na2HPO4.2H2O per L).
- Duration of treatment / exposure:
- 3 days
- Remarks:
- Doses / Concentrations:
2000 ppm
Basis:
nominal conc. - Control animals:
- yes, concurrent vehicle
- Positive control(s):
- ethyl methane sulfonate: post-meiotic germ cell stages
dimethylnitrosamine: pre-meiotic germ cell stages - Sex:
- male
- Genotoxicity:
- negative
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
- Conclusions:
- Interpretation of results (migrated information): negative
Genetic testing of acetaldehyde oxime in the Drosophila melanogaster sex-linked recessive lethal test indicates that it is not mutagenic in this organism. There is evidence, however, that AAO may have induced a significant level of sterility in the treated males. - Executive summary:
In the original study on post-meiotic germ cells a cluster of 8 mutants was recovered in the acetyldehyde oxime (AAO) series. In general terms, a cluster constitutes more than one lethal mutation recovered from an individual treated male. In instances where the overall mutation frequency is low, as in the present study, it is not clear that such clusters represent independent mutational events or that they result from a clone of germ cells carrying a prior formed spontaneous mutation. In the former case the mutations would be dispersed over the length of the X chromosome whereas in the latter case they would all occur at the same genetic locus. Unfortunately, the SRLR test does not possess the capability to detect which of these two alternatives is the true situation. When the cluster of 8 was considered as 8 independent events the frequency of mutations in the AAO treated series was significantly elevated above the control frequency. On the other hand, when the cluster was treated as a single prior event the effect of AAO was not significant. The equivocal nature of these data necessitated repeating the experiment. When the data of the second experiment are pooled with those of the first experiment a statistical analysis indicates that AAO did not induce a significant number of mutations. This is true whether the cluster is treated as 8 independent events or a single prior event.
In order to further substantiate that AAO is not mutagenic in higher eukaryotes it was decided to ascertain what effect, if any, it had on spermatogonial cells. These cells are considered to be at highest risk in males because they can accumulate genetic damage over the life time of the organism. Furthermore, they are physiologically different from the post meiotic germ cells in that they are continuously undergoing cell proliferation.
The data clearly show AAO to be non-mutagenic in Drosophila spermatogonial cells. An additional observation that deserves mention, however, is the fact that approximately 23% of the males on test with AAO exhibited complete sterility. This compares to a frequency of 6% in the negative control and is significant.
Reference
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
Genetic toxicity was evaluated in ten in vitro tests and in four in vivo tests. The in vitro tests comprise four bacterial reverse mutation tests (Simmon 1975; Rogers-Back et al. 1988; 1979; Wudl 1980), three in vitro mammalian cell gene mutation tests (Allied Chemical 1979; Stetka 1981; Rogers-Back et al. 1988), an unscheduled DNA synthesis (UDS) test (Williams 1985), asister chromatic exchange (SCE) test (Stetka 1981) and an alkaline elution test (Williams 1980). The four in vivo study reports comprise a sex-linked recessive lethal test (Brewen 1981), an in vivo SCE (Stetka 1981), an in vivo cytogenetic test (Brewen 1981) and a mouse dominant lethal test (Wudl 1980).
Four bacterial reverse mutation tests were conducted (Wudl 1980; Rogers-Back et al. 1988; Simmon 1975; Allied Chemical 1979). The results are summarized in the table below.
|
TA98 |
TA100 |
TA1535 |
TA1537 |
TA1538 |
|||||
|
- S9 |
+S9 |
-S9 |
+S9 |
-S9 |
+S9 |
-S9 |
+S9 |
-S9 |
+S9 |
Simmon 1975 |
- |
- |
- |
- |
- |
- |
- |
- |
- |
- |
Allied Chemical 1979 |
- |
- |
- |
- |
+ |
+ |
- |
- |
- |
- |
Wudl 1980 |
nc |
- |
- |
+ |
+ |
nc |
nc |
|||
Rogers-Back et al. 1988 |
- |
- |
- |
- |
- |
- |
- |
- |
- |
- |
nc: not conducte
In two tests (Simmon 1975; Rogers-Back et al. 1988) all tested Salmonella typhimurium strains (TA98, TA100, TA1535, TA1538) scored negative with and without metabolic activation. In the two other tests (Allied Chemical 1979; Wudl 1980), one strain, TA1535, scored positive. S. typhimurium TA1535 has a GC base pair at the primary reversion site and is able to detect base-pair substitutions. A bacterial strain (e.g. TA102) that detects cross-linking agents was not included in the tests.
Three in vitro mammalian gene mutation studies were performed. Two studies (1979; Stetka 1981) used Chinese Hamster Ovary (CHO) cells to check the ability of AAO to induce mutations in the HPRT1 gene. A third study (Rogers-Back et al. 1988) used lymphoma cells to evaluate the mutation rate in the tk gene.
In the most recent HPRT study (Stetka 1981), the test compound was applied only without metabolic activation. It was concluded that AAO does not cause mutations at the HPRT locus in CHO cells under the conditions of this assay while the positive control generated a clear positive dose response. In the other HPRT study (1979), sporadic non-reproducible positive responses were observed at various dose levels of AAO. There was no clear demonstration of a dose-response.
In the mouse lymphoma L5178Y TK+/- assay (Rogers-Back et al. 1988), AAO was mutagenic in the absence and presence of metabolic activation.
An unscheduled DNA synthesis (UDS) test was performed with GM38 fibroblast and primary Syrian hamster embryo (SHE) cells (Williams 1985). The UDS test measures the DNA repair synthesis after excision and removal of a stretch of DNA containing the region of damage induced by chemical or physical agents. AAO did not reproducibly induce UDS in these mammalian cells in the dose range 0.01-10 mg/mL.
A sister chromatic exchange (SCE) test was conducted to detect reciprocal exchanges of DNA between two sister chromatids of a duplicating chromosome. Analysis of the results of this assay indicates that AAO induces SCEs both with and without metabolic activation (Stetka 1981). AAO is, however, a very weak SCE-inducer, as not even a doubling of the background SCE frequency was observed.
An alkaline elution test with and without the use of cytosine-1-β-D-arabinofuranoside (ara-C)was performed (Williams 1980). AAO alone did not reproducibly produce atypical alkaline elution patterns (a measure of DNA damage). DNA strand breakage was detected when AAO was incubated in the presence of ara-C to prevent resealing of strand breaks produced during DNA repair. A dose-response occurred under these conditions corresponding to a frequency of about 4-40 x 10-8 breaks per nucleotide or 400-4000 breaks per cell during 4 h incubation.
Overall, these in vitro results show no or a low level of DNA damage, which is repairable as judged by the alkaline elution experiments.
AAO tested negative in all four conducted in vivo tests, comprising two somatic (SCE (Stetka 1981) and cytogenetic test (Brewen 1981)) and two heritable germ cell mutagenicity tests (sex-linked recessive lethal (Brewen 1981) and mouse dominant lethal test (Wudl 1980)).
The rapid metabolisation and elimination observed in the toxicokinetic study and the low mutagenic potential of AAO observed in some of the in vitro tests provide an explanation for the non mutagenicity of AAO in all the conducted in vivo tests.
Since AAO tested negative in all four in vivo mutagenicity tests, including two somatic and two heritable germ cell mutagenicity tests, AAO is not classified as a germ cell mutagen.
Justification for selection of genetic toxicity endpoint
SLRD-1981 is selected as the key study regarding gene mutation.
For chromosome aberrations; cytogenetics mouse_1981 is the key study.
Justification for classification or non-classification
Since AAO tested negative in all four in vivo mutagenicity tests, including two somatic and two heritable germ cell mutagenicity tests, classification as a germ cell mutagen is not required.
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