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EC number: 215-215-7 | CAS number: 1313-99-1
- 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 vivo
Administrative data
- Endpoint:
- in vivo mammalian cell study: DNA damage and/or repair
- Remarks:
- Type of genotoxicity: DNA damage and/or repair
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Meets generally accepted scientific standards, well documented and acceptable for publication.
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:
- publication
- Title:
- Distinct Mechanisms of Oxidative DNA Damage Induced by Carcinogenic Nickel Subsulfide and Nickel Oxides
- Author:
- Kawanishi S, Oikawa S, Inoue S, Nishino K
- Year:
- 2 002
- Bibliographic source:
- Environmental Health Perspectives. 110 (S5): 789-791
Materials and methods
Test guideline
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- DNA damage was evaluated in cultured cells and in lungs of rats; no standardized guidelines were followed.
- GLP compliance:
- not specified
- Type of assay:
- other: 8-hydroxydeoxyguanosine
Test material
- Reference substance name:
- Nickel monoxide
- EC Number:
- 215-215-7
- EC Name:
- Nickel monoxide
- Cas Number:
- 1313-99-1
- Molecular formula:
- NiO
- IUPAC Name:
- oxonickel
- Details on test material:
- - Name of test material (as cited in study report): NiO
- Substance type: green and black
Constituent 1
Test animals
- Species:
- rat
- Strain:
- Wistar
- Sex:
- not specified
- Details on test animals or test system and environmental conditions:
- Not reported.
Administration / exposure
- Route of administration:
- intratracheal
- Vehicle:
- - Vehicle(s)/solvent(s) used: no data
- Details on exposure:
- Noty applicable.
- Duration of treatment / exposure:
- acute
- Frequency of treatment:
- single
- Post exposure period:
- 48 hr
Doses / concentrations
- Remarks:
- Doses / Concentrations:
1 mg
Basis:
nominal conc.
- No. of animals per sex per dose:
- 4 to 9
- Control animals:
- yes
- Positive control(s):
- Not applicable.
Examinations
- Tissues and cell types examined:
- Lung tissue
- Details of tissue and slide preparation:
- Not applicable.
METHOD OF ANALYSIS:
Defrosted lungs were gently homogenized in 3 mL of PBS. The nuclei were obtained by centrifugation at 1,750×g for 5 min. For isolation of DNA, nucleic acid extraction system (model 341; Gene Pure, Applied Biosystems, Foster City, CA, USA) was used. DNA isolation was performed under helium. The content of 8-OH-dG was determined after enzyme digestion of DNA using an HPLC–ECD.
- Evaluation criteria:
- Not reported.
- Statistics:
- Not reported.
Results and discussion
Test results
- Sex:
- not specified
- Genotoxicity:
- positive
- Toxicity:
- not specified
- Vehicle controls validity:
- valid
- Negative controls validity:
- not examined
- Positive controls validity:
- not examined
- Additional information on results:
- see Table.
Any other information on results incl. tables
8 -OH-dG/dG x 10^5 in Rat Lung |
|||
Mean | SD | N | |
Control | 0.78 | 0.51 | 9 |
NiO black | 2.33* | 0.55 | 4 |
NiO green | 2.33* | 0.61 | 5 |
*, p < 0.01
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): positive
The authors posited that the in vivo damage could be explained by evidence that NiO causes inflammation and that inflammation subsequently causes the DNA damage. - Executive summary:
Kawanishi et al. (2002) measured 8-hydroxydeoxyguanosine (8-OH-dG) adducts in lung tissues of Wistar rats sacrificed 48 hours after exposure to 1 mg of various nickel compounds, including both black and green nickel oxides, via intratracheal instillation. Lungs were harvested, homogenized, and nuclei isolated by centrifugation. DNA was isolated and analyzed for 8-OH-dG by enzyme digestion and HPLC-ECD (high performance liquid chromatography-electrochemical detection). Relative to control cells, both black and green NiO increased DNA damage from approximately 0.78 to 2.33 8-OH-dG/dG×105. In contrast, neither NiO induced 8-OH-dG damage in vitro (see the Genetic Toxicity In Vitro section). The authors posited that the in vivo damage could be explained by previous studies that indicate NiO causes inflammation and that inflammation subsequently causes the DNA damage. However, the findings of this study are difficult to interpret given that only a single dose was administered via a non-environmentally relevant route and only a single species was evaluated. STUDY RATED BY AN INDEPENDENT REVIEWER
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