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Diss Factsheets
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EC number: 944-188-0 | 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
Neurotoxicity
Administrative data
- Endpoint:
- neurotoxicity
- Remarks:
- other: in vivo and in vitro studies
- Type of information:
- experimental study
- Adequacy of study:
- other information
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: special investigation
Data source
Reference
- Reference Type:
- publication
- Title:
- Neurotoxic potential of iron oxide nanoparticles in the rat brain striatum and hippocampus
- Author:
- Wu J, Ding T, Sun J
- Year:
- 2 013
- Bibliographic source:
- NeuroToxicology 34 (2013) 243–253
Materials and methods
- Principles of method if other than guideline:
- The study focuses on the effects of Fe3O4-NPs on the striatum and hippocampus, including oxidative injury and the accumulation and retention of Fe3O4-NPs. The study also explores the molecular mechanism of oxidative damage in dopaminergic neurons.
- GLP compliance:
- no
Test material
- Reference substance name:
- Reference substance 001
- Test material form:
- solid: nanoform
- Details on test material:
- The Fe3O4-NPs employed in this study were measured by TEM to be 30 nm in size (Fig. 2A) and remained spherical after being labelled with 125I. The hydrodynamic diameters of the Fe3O4-NPs and 125I-Fe3O4-NPs in physiological saline were 496+/- 86 nm and 462+/-75 nm, respectively. Zeta potential determination revealed that the Fe3O4-NPs and 125I-Fe3O4-NPs were 9.1+/- 2.2 mV and 8.4+/- 2.1 mV in physiological saline, respectively. Statistical comparisons showed no significant increases in size or zeta potential in the labelled particles (p > 0.05).
Constituent 1
Test animals
- Species:
- rat
- Strain:
- other: SD
- Sex:
- male
Administration / exposure
- Route of administration:
- other: intranasal
- Vehicle:
- physiological saline
- Duration of treatment / exposure:
- The rats in our studies were divided into four groups:
(1) intranasally instilled with 125I-Fe3O4-NPs for 1 day (In1d, euthanised at 1 d);
(2) intranasally instilled with 125IFe3O4-NPs for 7 days (In7d, euthanised at 8 d);
(3) 7 days postinstillation (post in 7d, euthanised at 14 d);
(4) 14 days postinstillation (post in 14d, euthanised at 21 d) - Frequency of treatment:
- The rats in our studies were divided into four groups:
(1) intranasally instilled with 125I-Fe3O4-NPs for 1 day (In1d, euthanised at 1 d);
(2) intranasally instilled with 125IFe3O4-NPs for 7 days (In7d, euthanised at 8 d);
(3) 7 days postinstillation (post in 7d, euthanised at 14 d);
(4) 14 days postinstillation (post in 14d, euthanised at 21 d)
- No. of animals per sex per dose:
- Six animals were euthanised at each time point (2 d, 8 d, 14 d, and 21 d)
Results and discussion
Any other information on results incl. tables
A regional distribution of Fe3O4-NPs was observed in rat brains after the particles were intranasally instilled for seven days. The particles were found to be deposited at particularly high concentrations in the rat striata and hippocampi. Over half of the Fe3O4-NPs were retained in the striata for a minimum of 14 days, and may have induced oxidative damage to the region. However, no injuries were observed in the hippocampi. These in vitro studies demonstrate that Fe3O4-NPs may decrease neuron viability, trigger oxidative stress, and activate JNK- and p53-mediated pathways to regulate the cell cycle and apoptosis. These results also suggest that environmental exposure to Fe3O4-NPs may play a role in the development of neurodegenerative diseases.
Applicant's summary and conclusion
- Executive summary:
This study focuses on the effects of Fe3O4-NPs on the striatum and hippocampus, including oxidative injury and the accumulation and retention of Fe3O4-NPs. This study also explores the molecular mechanism of oxidative damage in dopaminergic neurons.
A regional distribution of Fe3O4-NPs was observed in rat brains after the particles were intranasally instilled for seven days. The particles were found to be deposited at particularly high concentrations in the rat striata and hippocampi. Over half of the Fe3O4-NPs were retained in the striata for a minimum of 14 days, and may have induced oxidative damage to the region. However, no injuries were observed in the hippocampi. These in vitro studies demonstrate that Fe3O4-NPs may decrease neuron viability, trigger oxidative stress, and activate JNK- and p53-mediated pathways to regulate the cell cycle and apoptosis. These results also suggest that environmental exposure to Fe3O4-NPs may play a role in the development of neurodegenerative diseases.
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