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EC number: 231-673-0 | CAS number: 7681-57-4
- 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: sub-chronic oral
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Well-documented study of metabisulphite effects on cognitive function.
Cross-reference
- Reason / purpose for cross-reference:
- reference to same study
Data source
Reference
- Reference Type:
- publication
- Title:
- Effect of sulfite on cognitive function in normal and sulfite oxidase deficient rats.
- Author:
- Kücükatay, V.; et al.
- Year:
- 2 005
- Bibliographic source:
- Neurotox. Teratol. 27, 47-54
Materials and methods
Test guideline
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- Metabisulfite effects on cognitive function were studied in adult male albino rats and sulfite oxidase-deficient rats. Groups of adult male albino rats were treated as follows: drinking water with Na2S2O5 (25 mg/kg), vitamin E, and Na2S2O5 plus vitamin E. These treatments were for 6 weeks. A 4th group served as control. The same set of experiments was performed on sulphite oxidase-deficient (SOXD) rats. Active avoidance behaviour was studied. Prior to this, motor function of the rats was tested using the Hanging Wire Test. At the end, blood was collected for determination of plasma S-sulphonate levels. After exsanguination brain and liver tissues were removed immediately for measuring hippocampus TBARS levels and assay of SOX activity, respectively.
- GLP compliance:
- not specified
- Limit test:
- no
Test material
- Reference substance name:
- Disodium disulphite
- EC Number:
- 231-673-0
- EC Name:
- Disodium disulphite
- Cas Number:
- 7681-57-4
- Molecular formula:
- Na2S2O5
- IUPAC Name:
- disodium disulphite
- Details on test material:
- - Name of test material (as cited in study report): sodium metabisulfite
- Molecular formula (if other than submission substance):Na2S2O5
- Molecular weight (if other than submission substance): 190.1 g/mol
- Substance type: technical product
- Physical state: solid, white powder
No further details are given.
Constituent 1
Test animals
- Species:
- rat
- Strain:
- not specified
- Sex:
- male
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: breeding colony of the tet laboratory
- Age at study initiation: adult
- Weight at study initiation: 180-200 g
- Housing: four to five per cage
- Diet (ad libitum): standard rat chow for normal rast and Low-Mo-diet for SOX-deficient rats
- Water (ad libitum): tap water
ENVIRONMENTAL CONDITIONS
- Temperature (°C): 22 - 25 °C
- Photoperiod (hrs dark / hrs light): 12/12
Administration / exposure
- Route of administration:
- oral: drinking water
- Vehicle:
- water
- Remarks:
- and olive oil administered to the groups not receiving vitamin E
- Details on exposure:
- PREPARATION OF DOSING SOLUTIONS:
- group 1: drinking water with Na2S2O5 (25 mg/kg*d)
- group 2: vitamin E (50 mg/kg*d dissolved in olive oil given via gastric gavage)
- group 3: drinking water with Na2S2O5 (25 mg/kg*d) plus vitamin E (50 mg/kg*d dissolved in olive oil given via gastric gavage)
- group 4: controls
The same set of experiments was performed on sulphite oxidase-deficient (SOXD) rats. The SOX deficiency was produced by a low molybdenum diet and concurrent addition of 200 ppm sodium tungstate to their drinking water starting 3 weeks before sulphite and vitamin E dosing. - Analytical verification of doses or concentrations:
- not specified
- Duration of treatment / exposure:
- 6 weeks
Doses / concentrations
- Remarks:
- Doses / Concentrations:
25 mg/kg*d Na2S2O5
Basis:
nominal in water
- No. of animals per sex per dose:
- 10 animals each group (40 SOX-competent and 40 SOX-deficient, each divided into four subgroups)
- Control animals:
- yes
- Details on study design:
- - Rationale for animal assignment: randomly
Examinations
- Observations and clinical examinations performed and frequency:
- CAGE SIDE OBSERVATIONS: Yes
- Time schedule: no data
DETAILED CLINICAL OBSERVATIONS: Yes / No / No data
- Time schedule:
BODY WEIGHT: Yes
- Time schedule for examinations: no data
FOOD CONSUMPTION AND COMPOUND INTAKE (if feeding study):
- Food consumption for each animal determined and mean daily diet consumption calculated as g food/kg body weight/day: No data
- Compound intake calculated as time-weighted averages from the consumption and body weight gain data: No data
WATER CONSUMPTION AND COMPOUND INTAKE (if drinking water study): No data
OPHTHALMOSCOPIC EXAMINATION: No data
OTHER:
- At the end of the 6th week, blood was collected from the abdominal aorta under urethane anesthesia for determination of plasma S-sulphonate levels. Plasma S-sulphonate levels were measured as a biomarker for ingested sulfite according to the method of Gunnison et al (1987) - Neurobehavioural examinations performed and frequency:
- MOTOR FUNCTION TESTING
- motor function of the rats was tested using the Hanging Wire Test before starting active avoidance responses measurements
ACTIVE AVOIDANCE RESPOSES AND THE ACTIVE LEVELS
- Active avoidance behaviour was studied in the middle of the 6th week.
- each rat was given 50 trials of the procedure daily for 5 days
- the results were expressed as the mean percent avoidance responses for each daily shuttle box session - Sacrifice and (histo)pathology:
- - Time point of sacrifice: after 6 weeks of exposure, after blood collection
- Number of animals sacrificed: all animales
- Tissues evaluated:
After exsanguination brain and liver tissues were removed immediately for measuring hippocampus TBARS levels and assay of SOX activity in the livers, respectively. Hippocampus TBARS levels, an indicator of lipid peroxidation, were measured to determine if sulfite causes lipid peroxidation and in this manner induces neurotoxicity accordingt o the method of Winterbourn, et al (1985). Hepatic SOX activity was determined as an indicator of SOX status of the body according to the method of Cohen et al (1971). - Statistics:
- Results were expressed as means +/- S.E. Statistical comparison for repeated measurements between groups were made by repeated measures ANOVA for multiple comparisons, followed by TUKEY post hoc test. Differences between mean values in study groups were evaluated by a one-way ANOVA followed by TUKEY post hoc test. P values <0.05 were accepted as statistically significant.
Results and discussion
Results of examinations
- Clinical signs:
- no effects observed
- Mortality:
- no mortality observed
- Body weight and weight changes:
- no effects observed
- 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
- Clinical biochemistry findings:
- not specified
- Behaviour (functional findings):
- effects observed, treatment-related
- Description (incidence and severity):
- only in sulphite oxidase-deficient rats
- Gross pathological findings:
- not specified
- Neuropathological findings:
- not specified
- Details on results:
- CLINICAL SIGNS AND MORTALITY
- There were no signs of toxicity in any of the experimental groups.
- Treatment groups in both series exhibited similar survival.
BODY WEIGHT AND WEIGHT GAIN
- Treatment groups in both series exhibited similar weight gain.
NEUROBEHAVIOUR
- Rats of all groups did not have any motor coordination and balance abnormalities.
- Na2S2O5 induced impairment of active avoidance learning in sulphite oxidase-deficient rats but not in normal rats.
- Vitamin E did not reverse the acvtive avoiding learning in the sulphite oxidase-deficient rats
OTHER FINDINGS
- plasma S-sulphonate level was found to be increased significantly in all sulfite exposed groups by adding sulfite to the drinking water; vitamin E had no effect on this parameter [F(3,19) = 9,23, p<0.001]
- Metabisulphite had no effect on hippocampus TBARS levels in normal rats.
- However, the TBARS levels were significantly increased by metabisulphite in the enzyme-deficient rats.
- Vitamin E reversed the observed detrimental neurotoxic effects of metabisulphite in the sulphite oxidase-deficient rats on their hippocampal TBARS
Effect levels
- Dose descriptor:
- NOAEL
- Remarks on result:
- not determinable
- Remarks:
- no NOAEL identified
Applicant's summary and conclusion
- Conclusions:
- In conclusion, the studied sodium metabisulphite exposure has neurotoxic effects in sulphite oxidase-deficient rats, but not in normal rats. This effect may not depend on oxidative stress.
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