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EC number: 236-743-4 | CAS number: 13472-45-2
- 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
Description of key information
The neurotoxicity potential of sodium tungstate is reported by two publications by Sachdeva et al 2015 and Radcliffe et al 2009. An inhalation study reported that sodium tungstate is not appreciably transported via the olfactory pathway to the brain following a single 90-min exposure in rats, although this pathway is known to transport a number of other metals (Radcliffe et al, 2009). Sodium tungstate exposure was reported in one study to produced oxidative stress in brains from rats exposed. However, the study did not elucidate and correlate these oxidative changes with behavioral and functional alterations (Sachdeva et al, 2015).
Key value for chemical safety assessment
Effect on neurotoxicity: via oral route
Link to relevant study records
- Endpoint:
- neurotoxicity: short-term oral
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- study well documented, meets generally accepted scientific principles, acceptable for assessment
- Remarks:
- Well documented scientfically sound study with sufficient information provided on materials and methods to evaluate results.
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- The effects of sodium tungstate on oxidative stress, few selected neurological variables like acetylcholinesterase, biogenic amines in rat brain regions (cerebral cortex, hippocampus and cerebellum)
- GLP compliance:
- not specified
- Remarks:
- Study has adequate and reliable coverage of the key parameters foreseen to be investigated in the corresponding test methods and adequate and reliable documentation of the study is provided
- Limit test:
- yes
- Species:
- rat
- Strain:
- Wistar
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- Male Wistar rats, weighing approximately 100–120 g were used in the study. Prior to the dosing, they were acclimatized for 7 days. Briefly, animals were kept in polypropylene cages with clean dust free rice husk. The animals were housed in stainless steel cages in an air-conditioned room with temperature maintained at 25 ± 2 °C and relative humidity 60 ± 10%. Animals’ rooms were illuminated with 300 lux light, alternating with 12 h darkness light from 06:00 to 18:00 h and vice versa. Rats were allowed standard chow diet throughout the experiment and water ad libitum.
- Route of administration:
- oral: drinking water
- Vehicle:
- water
- Details on exposure:
- Rats were divided into eight groups of 10 rats each and were treated as below for 3 months (five days a week):
Group I: Normal animal, received normal water
Group II: Sodium tungstate, 100 ppm in drinking water, daily
Group III: Quercetin alone, orally, once, daily (0.30 mM)
Group IV: N-acetylcysteine (NAC) alone, orally, once, daily (0.30 mM)
Group V: Flavonoid (naringenin) alone, orally, once, daily (0.30 mM)
Group VI: Sodium tungstate + Quercetin as in group II and group III, respectively
Group VII: Sodium tungstate + NAC (as in group II + group IV, respectively)
Group VIII: Sodium tungstate + Flavonoid (naringenin) (as in group II + group V, respectively) - Analytical verification of doses or concentrations:
- not specified
- Duration of treatment / exposure:
- 90 days
- Frequency of treatment:
- Daily
- Dose / conc.:
- 100 ppm
- Remarks:
- nominal in water
- No. of animals per sex per dose:
- 10 rats per group
- Control animals:
- yes, concurrent vehicle
- Specific biochemical examinations:
- - Amount of reactive oxygen species in blood was measured using 2′, 7′-dichlrofluorescein diacetate (DCF-DA) that gets converted into highly fluorescent DCF by cellular peroxides (including hydrogen peroxide). The supernatant fractions obtained were used to determine the following parameters in three different brain regions:
- Measurement of lipid peroxidation was conducted by the thiobarbituric acid reactive substances (TBARS).
- Tissue reduced glutathione (GSH) and oxidized glutathione (GSSG)
- Tissue glutathione peroxidase (GPx)
- Tissue glutathione-S-transferase (GST
- Brain acetyl cholinesterase (AChE) activity
- Brain monoamine oxidase (MAO) activity
- Brain biogenic amine levels (dopamine and nor epinephrin) - Neurobehavioural examinations performed and frequency:
- None
- Sacrifice and (histo)pathology:
- Brains were quickly dissected out, placed on a glass plate resting over crushed ice for the separation of various regions (cortex, cerebellum and hippocampus). The brain parts were homogenized in phosphate buffer (pH 7.4).
- Statistics:
- The results are expressed as the mean ± SEM of number of observations. Comparisons of means were carried out using ANOVA followed by Bonferroni multiple comparison test to compare means between the different treatment groups
- Clinical signs:
- not specified
- Mortality:
- no mortality observed
- Body weight and weight changes:
- not specified
- Food consumption and compound intake (if feeding study):
- not specified
- Food efficiency:
- not specified
- Water consumption and compound intake (if drinking water study):
- not specified
- Ophthalmological findings:
- not specified
- Haematological findings:
- not specified
- Clinical biochemistry findings:
- effects observed, treatment-related
- Description (incidence and severity):
- Significant increase in oxidative stress variables.
- Urinalysis findings:
- not specified
- Behaviour (functional findings):
- not specified
- Immunological findings:
- not specified
- Organ weight findings including organ / body weight ratios:
- not specified
- Gross pathological findings:
- not specified
- Neuropathological findings:
- not specified
- Histopathological findings: non-neoplastic:
- not specified
- Histopathological findings: neoplastic:
- not specified
- Other effects:
- effects observed, treatment-related
- Description (incidence and severity):
- - Brain ROS increased significantly in the cortex and hippocampus; however, an increasing trend was noticed in the cerebellum of rats on sodium tungstate exposure compared to normal animals.
- increase in GPXactivity in cerebellum compared to cortex and hippocampus on sodium tungstate exposure. GST activity on the other hand, significantly decreased in cortex, cerebellum and hippocampus.
- Depletion of dopamine (DA) in cortex and cerebellum was observed in sodium tungstate exposed rats as compared to normal control rats.
- Following sodium tungstate exposure, 5-HT levels were depleted in the cortex and marginally in the cerebellum.
- Sodium tungstate exposure produced an increase in Nor Epinephrie (NE) levels in hippocampus while there was a significant reduction in cortex and marginal fall in cerebellum compared to the NE levels of control rats.
- Sodium tungstate exposed animals showed an alteration in AChE activity in cortex and cerebellum compared to hippocampus.
- Sodium tungstate exposed animals showed a more pronounced alteration in AChE activity in cortex and cerebellum compared to hippocampus
- Co-administration of NAC and flavonoids with tungstate provided moderately effective in reducing brain ROS, moderately prevent effects in restoring GPX and GST activities in the different brain regions, recover the altered DA levels in cortex and cerebellum; and provided a significant recovery in the 5-HT level of the cortex and hippocampus, restored the altered NE levels in all the brain regions, and increase in the activity of acetylcholinesterase. - Key result
- Dose descriptor:
- conc. level:
- Effect level:
- 100 ppm (nominal)
- Based on:
- test mat.
- Sex:
- male
- Basis for effect level:
- other: Tungstate exposure produced an increase in biochemical variables indicative of oxidative stress but no correlation was conducted with behavioral and functional alteration.
- Remarks on result:
- not determinable
- Conclusions:
- Tungstate exposure produced an increase in biochemical variables indicative of oxidative stress while, neurological alterations were more pronounced in the cerebral cortex compared to other regions. Co-administration of NAC and flavonoids with sodium tungstate significantly restored glutathione, prevented changes in the brain biogenic amines, reactive oxygen species (ROS) and TBARS levels in the different brain regions. The protection was more prominent in the animals co-administered with NAC. Further studies are required for elucidating and correlating the behavioral and functional alterations.
Reference
Endpoint conclusion
- Endpoint conclusion:
- no study available
Effect on neurotoxicity: via inhalation route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Effect on neurotoxicity: via dermal route
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Justification for classification or non-classification
The sodium tungstate neurotoxicity studies are more investigative reports conducted under no standard testing guidelines which limit their usability for regulatory purposes. Based on this, none of the data from these publications warrant any classification for sodium tungstate as a neurotoxicant per CLP as more information is needed.
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