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EC number: 941-652-4 | CAS number: -
- 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 gene mutation study in mammalian cells
- Remarks:
- Type of genotoxicity: gene mutation
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- July 2008 to October 2008
- Reliability:
- 1 (reliable without restriction)
- Rationale for reliability incl. deficiencies:
- other: Guideline study
Cross-referenceopen allclose all
- Reason / purpose for cross-reference:
- reference to same study
- Reason / purpose for cross-reference:
- reference to other study
Data source
Reference
- Reference Type:
- study report
- Title:
- Unnamed
- Year:
- 2 008
- Report date:
- 2008
Materials and methods
Test guideline
- Qualifier:
- according to guideline
- Guideline:
- OECD Guideline 476 (In Vitro Mammalian Cell Gene Mutation Test)
- GLP compliance:
- yes
- Type of assay:
- mammalian cell gene mutation assay
Test material
- Reference substance name:
- pentanickel dicarbonate hexahydroxide
- Cas Number:
- 12122-15-5
- Molecular formula:
- C2H6Ni5O12
- IUPAC Name:
- pentanickel dicarbonate hexahydroxide
- Details on test material:
- - Name of test material (as cited in study report): Nickel hydroxycarbonate
- Substance type: pure product
- Physical state: green powder
- Analytical purity: 100%
- Stability under test conditions: Stable
- Storage condition of test material: room temperature, closed container
Constituent 1
Method
- Target gene:
- Thymidine Kinase (TK) locus
Species / strain
- Species / strain / cell type:
- mouse lymphoma L5178Y cells
- Details on mammalian cell type (if applicable):
- - Type and identity of media: RPMI + 3% horse serum, or + 7.5% horse serum for long-term exposure
- Properly maintained: yes
- Periodically checked for Mycoplasma contamination: not reported
- Periodically checked for karyotype stability: yes
- Periodically "cleansed" against high spontaneous background: yes - Additional strain / cell type characteristics:
- not specified
- Metabolic activation:
- with and without
- Metabolic activation system:
- S9
- Test concentrations with justification for top dose:
- Experiment I: with metabolic activation: 10, 40, 80, 110, 140, 170, 200, 230 ug/mL
Experiment I: without metabolic activation: 10, 20, 40, 60, 80, 110, 140, 170 ug/mL
Experiment II: with metabolic activation: 40, 80, 100, 120, 140, 160, 200, 220 ug/mL
Experiment II: with metabolic activation: 1, 2, 5, 10, 17.5, 25, 32.5, 40 ug/ml - Vehicle / solvent:
- - Vehicle(s)/solvent(s) used: [medium]
Controls
- Untreated negative controls:
- yes
- Negative solvent / vehicle controls:
- yes
- True negative controls:
- not specified
- Positive controls:
- yes
- Positive control substance:
- other: EMS or MMS
- Details on test system and experimental conditions:
- METHOD OF APPLICATION: in medium
DURATION
- Preincubation period: 1-3 days
- Exposure duration: 4 or 24 hours
- Expression time (cells in growth medium): 48 or 72 hours
NUMBER OF CELLS EVALUATED: 200 cells per well in four 96 wells
DETERMINATION OF CYTOTOXICITY
- Method: relative total growth
- Evaluation criteria:
- Positive results based on clear dose related mutant frequency and biologically relevant response.
- Statistics:
- no statistics performed
Results and discussion
Test results
- Species / strain:
- mouse lymphoma L5178Y cells
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- valid
- Positive controls validity:
- valid
- Additional information on results:
- ADDITIONAL INFORMATION ON CYTOTOXICITY:
-Growth inhibition was observed with and without metabolic activation.
-pH was within the physiological range - Remarks on result:
- other: all strains/cell types tested
- Remarks:
- Migrated from field 'Test system'.
Applicant's summary and conclusion
- Conclusions:
- Nickel hydroxycarbonate is considered to be non-mutagenic in the mouse lymphoma thymidine kinase locus assay.
- Executive summary:
BSL (2008) performed a study using the mouse lymphoma cell line L5178Y to assess the potential for nickel hydroxycarbonate to cause gene mutations in vitro. Genetic damage was assessed with the thymidine kinase assay (carried out according to OECD Guideline 476 and using GLP standards). Two separate experiments were conducted, both with and without metabolic activation using a S9 mix. Based on results obtained from a pre-experiment, the exposure concentrations were as follows: Experiment I with metabolic activation (10, 40, 80, 110, 140, 170, 200, and 230 μg/mL), without metabolic activation (10, 20, 40, 60, 80, 110, 140,and 170 μg/mL); Experiment II with metabolic activation (40, 80, 100, 120, 140, 160, 200, and 220 μg/mL), without metabolic activation (1, 2, 5, 10, 17.5, 25, 32.5, and 40 μg/mL). In Experiment II without metabolic activation, cells were exposed for 24 hours as a long-term exposure assay; the other experiments used a 4-hour exposure period. Negative controls (vehicle only) and positive controls(ethylmethanesulfonate, methylmethanesulfonate [both without metabolic activation]; benzo[a]pyrene [with metabolic activation]) were used in the study.
For each experiment, mutagenicity, toxicity (measured as growth inhibition), and colony size (to determine clastogenic effects) data were collected. No biologically significant increase in mutation frequencies occurred following nickel hydroxycarbonate treatment, for either experiment and under conditions with or without metabolic activation. Growth inhibition occurred in Experiments I and II, under conditions with and without metabolic activation. The relative total growth (RTG) findings with the corresponding highest concentrations evaluated were as follows: Experiment I with metabolic activation (13.49% for 230 μg/mL), Experiment I without metabolic activation (13.43% for 170 μg/mL), Experiment II with metabolic activation (17.12% for 220 ug/mL), Experiment II without metabolic activation (12.67%. for 40 ug/mL). No clastogenic effects occurred following nickel hydroxycarbonate treatment, for either
experiment and under conditions with or without metabolic activation. The authors concluded that, using the cell line L5178Y, nickel hydroxycarbonate was non-mutagenic at the mouse lymphoma thymidine kinase locus.
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