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EC number: 222-392-4 | CAS number: 3458-28-4
- 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
Developmental toxicity / teratogenicity
Administrative data
- Endpoint:
- developmental toxicity
- Type of information:
- experimental study
- Adequacy of study:
- disregarded due to major methodological deficiencies
- Reliability:
- 3 (not reliable)
- Rationale for reliability incl. deficiencies:
- significant methodological deficiencies
Data source
Reference
- Reference Type:
- publication
- Title:
- Fuel-mediated teratogenesis: Symmetric growth retardation in the rat fetus at term after a circumscribed exposure to D-mannose during organogenesis
- Author:
- Buchanan TA and Freinkel N
- Year:
- 1 988
- Bibliographic source:
- Am. J. 0bstet. Gynecol., 158:663-669
Materials and methods
- Principles of method if other than guideline:
- Ten pregnant animals were infused with the test item for 12 hours during early neurulation (day 9.5 to 10 of development). Foetuses were removed at term and examined for evidence of developmental anomalies and growth retardation.
- GLP compliance:
- no
Test material
- Reference substance name:
- D-mannose
- EC Number:
- 222-392-4
- EC Name:
- D-mannose
- Cas Number:
- 3458-28-4
- Molecular formula:
- C6H12O6
- IUPAC Name:
- D-mannose
- Details on test material:
- Purity: not reported
Constituent 1
Test animals
- Species:
- rat
- Strain:
- other: Crl: CD [SD] BR
Administration / exposure
- Route of administration:
- infusion
- Vehicle:
- water
- Analytical verification of doses or concentrations:
- yes
- Details on mating procedure:
- Female rats were mated with normal males of the same strain. Midnight of the night of mating (confirmed by the presence of sperm in the vaginal smear the following morning) was designated day 0 of intrauterine development. Pregnant females were housed singly with free access to food and water except during infusions.
- Duration of treatment / exposure:
- days 9.5 and 10
- Frequency of treatment:
- continuous infusion between days 9.5 and 10
- Duration of test:
- At day 21.5 of development
- No. of animals per sex per dose:
- 10
- Control animals:
- other: d-glucose
Results and discussion
Results: maternal animals
Effect levels (maternal animals)
- Dose descriptor:
- other: developmental toxicity
- Effect level:
- >= 1.5 - <= 2 other: mg/mL
- Based on:
- test mat.
- Basis for effect level:
- other: developmental toxicity
Results (fetuses)
- Details on embryotoxic / teratogenic effects:
- Embryotoxic / teratogenic effects:yes
Fetal abnormalities
- Abnormalities:
- not specified
Overall developmental toxicity
- Developmental effects observed:
- not specified
Applicant's summary and conclusion
- Conclusions:
- These results indicate that a relatively brief metabolic insult to embryos during early organogenesis may cause lethal developmental anomalies as well as growth retardation and delayed skeletal development that are manifested in the foetus at term.
- Executive summary:
Ten pregnant animals were infused with d-mannose for 12 hours during early neurulation (day 9.5 to 10 of development). Ten control animals were infused with equimolar d-glucose during this same time interval.
Mannose infusions produced maternal plasma mananose concentrations in the embryotoxic range; glucose infusions caused only slight and transient hyperglycemia. None of 137 foetuses from the mannose group or 138 foetuses from the glucose group exhibited gross anomalies. However, an excess of resorbed conceptions in the mannose group (21 versus six in the glucose group; p < 0.01) suggested some lethal toxicity from mannose exposure during embryogenesis. Among viable foetuses, the mean body weight of those from the mannose group was significantly reduced compared with those from the glucose group (5.62 + 0.04 versus 5.89 + 0.03 gm, respectively; p < 0.001). Reductions of a similar magnitude were noted in the mean wet weight and protein content of foetal brains, hearts, livers, and kidneys from the mannose group (range, 3.4% to 7.1% below the glucose group), indicating a symmetric pattern of foetal growth retardation. In addition, analysis of foetal ossification sites after Alizarin Red S staining revealed a significant delay of skeletal development in the mannose group. These results indicate that a relatively brief metabolic insult to embryos during early organogenesis may cause lethal developmental anomalies as well as growth retardation and delayed skeletal development that are manifested in the foetus at term.
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