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EC number: 201-928-0 | CAS number: 89-65-6
- 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
Basic toxicokinetics
Administrative data
- Endpoint:
- basic toxicokinetics in vivo
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Final Report on the Safety Assessment of Ascorbyl Palmitate, Ascorbyl Dipalmitate, Ascorbyl Stearate,Erythorbic Acid, and sodium Erythorbate
- Author:
- F. Alan Andersen
- Year:
- 1 999
- Bibliographic source:
- International Journal of Toxicology
Materials and methods
Test guideline
- Guideline:
- other: Absorption, Distribution, Metabolism, and Excretion
- GLP compliance:
- not specified
Test material
- Reference substance name:
- 2,3-didehydro-D-erythro-hexono-1,4-lactone
- EC Number:
- 201-928-0
- EC Name:
- 2,3-didehydro-D-erythro-hexono-1,4-lactone
- Cas Number:
- 89-65-6
- Molecular formula:
- C6H8O6
- IUPAC Name:
- (5R)-5-[(1R)-1,2-dihydroxyethyl]-3,4-dihydroxy-2,5-dihydrofuran-2-one
- Test material form:
- solid: crystalline
Constituent 1
Administration / exposure
- Route of administration:
- oral: feed
Results and discussion
Main ADME resultsopen allclose all
- Type:
- absorption
- Type:
- distribution
- Type:
- metabolism
- Type:
- excretion
Toxicokinetic / pharmacokinetic studies
- Details on absorption:
- Homig (1977) reported that absorption was approximately four-to-one in favor of ascorbic acid, but the availability of ascorbic acid decreased by 40-60% when administered with Erythorbic Acid. Further data indicated that Erythorbic Acid promoted the acceleration of oxidative destruction of ascorbic acid in the liver.
Another study by Suzuki, Kurata, and Arakawa (1991) determined that Erythorbic Acid was absorbed less efficiently than ascorbic acid in the small intestine of male Hartley guinea pigs. The data also suggested that Erythorbic Acid was absorbed from the small intestine by the same active transport mechanism as used for ascorbic acid. The absorption rates of both in the small intestine could be dependent on the concentration of ascorbic acid already present in the tissues of the guinea pig. - Details on distribution in tissues:
- Erythorbic Acid was not transported in vivo into the brain, cerebrospinal fluid (Homig 1977), white blood cells, adrenal glands, and the globes as effectively as L-ascorbic acid.
In studies in which L-ascorbic acid intake was low, the greatest concentrations of Erythorbic Acid were in the liver, adrenal glands, spleen, and kidneys (Suzuki et al. 1986).
- Details on excretion:
- Tsao and Salimi (1983) gave 21 Swiss Webster female mice (4-week-old) feed containing 5% ascorbic acid or Erythorbic Acid crystals for 2 months. The mice (five per group) were then fed diet containing 10% ascorbic acid or Erythorbic Acid for 5 additional months. Eleven mice received ascorbic acid-free diet throughout the experiment. Urine was collected and analyzed 2 weeks before termination of the study. The mice were killed and their brains and livers were removed and stored for analysis. The amount of urinary Erythorbic Acid excreted from mice given Erythorbic Acid was approximately twice that of mice given ascorbic acid.
Erythorbic Acid apparently was not reabsorbed after glomerular filtration, and, therefore, was excreted from the kidneys more rapidly than L-ascorbic acid. In dogs, this resulted in a half-life of approximately 30 minutes for Erythorbic Acid in the plasma (Silber 1956). Wang, Fisher, and Dodds (1962) reported that Erythorbic Acid was excreted faster than L-ascorbic acid in humans.
Metabolite characterisation studies
- Details on metabolites:
- The reduced form of Erythorbic Acid was incorporated into human erythrocytes at the rate of 20% per 2 hours and the rate of uptake of this form was proportional to the extracellular concentration. The oxidized form of Erythorbic Acid, D-dehydroisoascorbic acid, became incorporated more rapidly than the reduced form, at a rate of 50% per 5 minutes, and 80% of the acid absorbed was subsequently reduced within the cells. The reduced form of Erythorbic Acid was more stable in plasma than the oxidized form, of which 61 % was degraded in 60 minutes. In erythrocytes, the reduced form was stable, as in plasma, and the oxidized form slightly less so (Teruuchi and Okamura 1972).
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): no bioaccumulation potential based on study results
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