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EC number: 240-841-2 | CAS number: 16812-54-7
- 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

Acute Toxicity: other routes
Administrative data
- Endpoint:
- acute toxicity: other routes
- 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:
- Superoxide radical and toxicity of environmental nickel exposure
- Author:
- Novelli ELB, Rodrigues NL, Ribas BO
- Year:
- 1 995
- Bibliographic source:
- Human & Experimental Toxicology. 14: 248-251
Materials and methods
Test guideline
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- 7 mg Ni/kg, in the form of NiS (nickel monosulfide), was administered to rats in a single i.m. injection. After 72 hours, serum activity levels of lipoperoxide, amylase, aspartate transaminase, alkaline phosphatase, glutathione peroxidase, and superoxide dismutase (SOD) were measured. Similar studies were repeated where animals were also treated with purified SOD and NiO.
- GLP compliance:
- not specified
- Limit test:
- no
Test material
- Reference substance name:
- Nickel sulphide
- EC Number:
- 240-841-2
- EC Name:
- Nickel sulphide
- Cas Number:
- 16812-54-7
- Molecular formula:
- NiS
- IUPAC Name:
- nickel(2+) sulfanediide
- Details on test material:
- - Name of test material (as cited in study report): NiS (nickel monosulfide)
Constituent 1
Test animals
- Species:
- rat
- Strain:
- Wistar
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Age at study initiation: 15 mo
- Weight at study initiation: 180-200 g
- Individual metabolism cages: no
- Diet (e.g. ad libitum): Food (Purina Ltd., 3074 SIF) ad libitum
- Water (e.g. ad libitum): ad libitum
Administration / exposure
- Route of administration:
- intramuscular
- Vehicle:
- physiological saline
- Details on exposure:
- Injections were made into the muscle (i.m.) of the right thigh, approximately parallel with the femur in 0.2 mL of 0.9%NaCl. Another group of animals were administered purified SOD conjugated to polyethylene glycol (SOD-PEG) via i.p. once daily following i.m. injection with NiO or hydroxylamine.
- Doses:
- 7 mg Ni/kg
- No. of animals per sex per dose:
- Males (numbers not reported).
- Control animals:
- yes
- Details on study design:
- - Duration of observation period following administration: single injection, 72 hr post-injection
- Frequency of observations and weighing: once
- Necropsy of survivors performed: no
- Other examinations performed: serum biomarkers - protein, lipoperoxide, alkaline phosphatase, amylase, aspartate transaminase, alanine transaminase, glutathione peroxidase, and superoxide dismutase. - Statistics:
- Values are presented as means ± s.d. Significance of difference was tested by Student's t-test (P < 0.05).
Results and discussion
Effect levels
- Sex:
- male
- Dose descriptor:
- other: significant change in serum markers
- Effect level:
- ca. 7 other: mg Ni/kg
- Remarks on result:
- other: lipoperoxides, amylase, AST, ALP, SOD
- Mortality:
- Not reported.
- Clinical signs:
- Not reported.
- Body weight:
- Not reported.
- Gross pathology:
- Not reported.
- Other findings:
- - Other observations: serum biomarkers - protein, lipoperoxide, alkaline phosphatase, amylase, aspartate transaminase, alanine transaminase, glutathione peroxidase, and superoxide dismutase.
Any other information on results incl. tables
Effects of NiS on Serum Markers
Control | NiS | Hydroxylamine | |
Total protein (g/dL) | 5.9 (0.8) | 5.9 (0.9) | 5.9 (1.2) |
Lipoperoxide (ueq/L) | 1.8 (0.7) | 5.8 (0.7)* | 9.8 (0.8)* |
Amylase (U/dL) | 60.8 (10.7) | 89.6 (2.8)* | 93.6 (3.1)* |
AST (U/mL) | 28.9 (9.2) | 58.9 (10.3)* | 50.7 (0.8)* |
ALT (U/mL) | 9.5 (0.6) | 8.9 (0.6) | 9.0 (1.6) |
ALP (mU/mL) | 63.5 (8.6) | 108.9 (9.8)* | 109.8 (8.5)* |
SOD (U/mL) | 0.56 (0.3) | 0.38 (0.07)* | 0.33 (0.1)* |
GSH-PX (U/mg protein) | 0.9 (0.1) | 0.9 (0.2) | 0.8 (0.3) |
*, Values are significantly different from those of the control group by Student's t-test (P < 0.05)
AST, aspartate transaminase; ALT, alanine transaminase; ALP, alkaline phosphatase; SOD, superoxide dismutase; GSH-PX, glutathione peroxidase; U, unit of activity
Additional Results:
1, similar findings were reported for NiO as for NiS
2, NiCl2 only increased AST
3, Administration of purified SOD had no significant effect on the parameters in the table in control animals; yet negated all of the significant effects from exposure to NiO, NiS, and hydroxylamine.
Applicant's summary and conclusion
- Conclusions:
- The authors concluded that the toxicity of nickel compounds involves oxidative reactions such as nickel induced lipid peroxidation, and that the superoxide radical is an important toxic intermediate in the development of insoluble nickel compound damage, since SOD-PEG has a potential therapeutic effect.
- Executive summary:
- Novelli et al. (1995) examined the ability of several Ni compounds, including NiS, to induce pancreatic, hepatic, and osteogenic lesions. The purpose of this study was to evaluate the toxicity of soluble and insoluble Ni compounds and the potential involvement of oxidative mechanisms. Male Wistar rats were administered a single i.m. injection of NiS at a dose of 7 mg Ni/kg. After 72 hours, NiS treated rats exhibited significant increases in serum lipoperoxide, amylase, aspartate transaminase, and alkaline phosphatase, as well as a significant decrease in superoxide dismutase (SOD). For comparison, animals were also injected with hydroxylamine as a means of inducing “superoxide flux.” Hydroxylamine increased lipoperoxide, alkaline phosphatase, amylase, and aspartate transaminase, decreased SOD, and caused no change in glutathione peroxidase. The similar responses between hydroxylamine and NiS were posited to reflect a similar mechanism of action. In this regard, another group of animals were administered purified SOD conjugated to polyethylene glycol (SOD-PEG) via i.p. once daily following i.m. injection with NiS or hydroxylamine. The animals did not show the aforementioned changes. Because SOD catalyses the destruction of superoxide radical and was shown to prevent significant change in the aforementioned parameters, the data suggest the involvement of oxidative mechanisms in the toxicity of NiS. The authors concluded that the toxicity of nickel compounds involves oxidative reactions such as nickel induced lipid peroxidation, and that the superoxide radical is an important toxic intermediate in the development of insoluble nickel compound-induced damage, since SOD-PEG has a potential therapeutic effect. STUDY RATED BY AN INDEPENDENT REVIEWER
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