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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
Genetic toxicity: in vitro
Administrative data
- Endpoint:
- in vitro DNA damage and/or repair study
- Remarks:
- Type of genotoxicity: DNA damage and/or repair
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- 1980-1981
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Well documented study.
Data source
Reference
- Reference Type:
- study report
- Title:
- Unnamed
- Year:
- 1 981
- Report date:
- 1981
Materials and methods
Test guideline
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 479 (Genetic Toxicology: In Vitro Sister Chromatid Exchange Assay in Mammalian Cells)
- GLP compliance:
- not specified
- Type of assay:
- sister chromatid exchange assay in mammalian cells
Test material
- Reference substance name:
- Acetaldehyde oxime
- EC Number:
- 203-479-6
- EC Name:
- Acetaldehyde oxime
- Cas Number:
- 107-29-9
- Molecular formula:
- C2H5NO
- IUPAC Name:
- acetaldehyde oxime
- Details on test material:
- - test material: acetaldehyde oxime (AAO)
- source: Sigma Chemical Company
- Lot No.: 290-0490
- Purity: 99.9% pure by HPLC
Constituent 1
Method
Species / strain
- Species / strain / cell type:
- Chinese hamster Ovary (CHO)
- Details on mammalian cell type (if applicable):
- - Type and identity of media: Ham's F12 with 10% filtered FBS and 1% antibiotic/antimycotic
- Metabolic activation:
- with and without
- Metabolic activation system:
- S9 metabolic system
- Test concentrations with justification for top dose:
- - Experiment 1: 0, 0.01, 0.03, 0.1, 0.3 μL/mL AAO
- Experiment 2: 0, 0.0006, 0.002, 006 μL/mL AAO
- Experiment 3: 0, 0.01, 0.03, 0.1, 0.3 μL/mL AAO
- Experiment 4: 0, 0.03, 0.06, 0.09 μL/mL AAO - Vehicle / solvent:
- water
Controls
- Negative solvent / vehicle controls:
- yes
- True negative controls:
- no
- Positive controls:
- yes
- Remarks:
- positive controls: benzo(a)pyrene, ethylnitrosourea
- Details on test system and experimental conditions:
- DURATION
- Exposure duration: 0.5 - 27 h
- Fixation time (start of exposure up to fixation or harvest of cells): 27 - 29 h
SPINDLE INHIBITOR: colcemid
STAIN: bromodeoxyuridine (BrdU)
DETERMINATION OF CYTOTOXICITY
- Method: determination of dividing cells
Results and discussion
Test results
- Species / strain:
- Chinese hamster Ovary (CHO)
- Metabolic activation:
- with and without
- Genotoxicity:
- positive
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information):
positive
Analysis of results from the sister chromatid exchange (SCE) assay in cultured mammalian Chinese hamster ovary cells indicates that acetaldehyde oxime (AAO) induces SCEs both with and without metabolic activation, and that it is somewhat more toxic or inhibitory, in terms of cell cycle progression, when used together with metabolic activation system. AAO is, however, a very weak SCE-inducer, as not even a doubling of the background SCE frequency was observed. - Executive summary:
Initial experiments were designed to determine, quite simply, whether or not acetaldehyde oxime (AAO) does or does not induce sister chromatid exchanges (SCEs) in vitro. Positive controls were not employed as there were intended to serve as preliminary, range-finding-type experiments. Low doses were employed in the activation test because previous work (conducted by other Allied personnel) had indicated an approximate 50 -fold increase in toxicity when AAO was used with the metabolic activation systems. While AAO proved to be positive with regard to SCE induction at these low doses, there was no indication of toxicity. Many second division cells were present, indicating that mitotic delay, if present, was not severe; and, in addition, very few dead, floating cells were present in the culture.
Experiment 3 re-tested AAO with the S9 activation system but employed higher doses. AAO was again positive with activation and toxicity was apparent at the highest doses.
The final experiment (No. 4) was intended to determine whether or not the small increases in SCE frequency observed with AAO are truly the result of AAO interactions with CHO DNA or might have been due to AAO toxicity, with the result that surviving cells incorporated more BrdU. It has been previously been reported that increases in the BrdU/cell ratio can increase SCE frequencies nearly 2 -fold. The experimental results indicate that in fact, while higher BrdU doses do lead to greater SCE frequencies, AAO does induce SCEs directly.
In conclusion, AAO induces SCEs both with and without metabolic activation. Metabolic activation has little or no effect on SCE induction, but does render AAO somewhat more toxic, as greater numbers of scorable mitotic cells were present at higher doses when the compound was used directly vis-a-vis use with the metabolic activation system.
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