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Diss Factsheets
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EC number: 200-718-6 | CAS number: 69-89-6
- 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
Acute Toxicity: inhalation
Administrative data
- Endpoint:
- acute toxicity: inhalation
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- data from handbook or collection of data
Data source
Reference
- Reference Type:
- publication
- Title:
- Airway inflammation induced by xanthine/xanthine oxidase in guinea pigs
- Author:
- M. Misawa and H. Arai
- Year:
- 1 993
- Bibliographic source:
- Agent Actions, 38:19-26
Materials and methods
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- Airway inflammation was assessed by airway vascular permeability in terms of Pontamine skyblue exudation. Vascular permeability was quantified by the extravasation of Pontamine sky-blue dye using a modified method of Evans et al. [T. W. Evans, K. F. Chung, D. F. Rogers and P. J. Barnes, Effect of platelet-activating factor on airway vascular permeability." possible mechanisms. J. Appl. Physiol. 63, 479 484 (1987)]
- GLP compliance:
- no
Test material
- Reference substance name:
- Purine-2(3H),6(1H)-dione
- EC Number:
- 200-718-6
- EC Name:
- Purine-2(3H),6(1H)-dione
- Cas Number:
- 69-89-6
- Molecular formula:
- C5H4N4O2
- IUPAC Name:
- xanthine
Constituent 1
- Specific details on test material used for the study:
- Purity: not reported
Test animals
- Species:
- guinea pig
- Strain:
- Hartley
- Sex:
- male
Administration / exposure
- Route of administration:
- inhalation: aerosol
- Type of inhalation exposure:
- whole body
- Duration of exposure:
- 5 min
- Remarks on duration:
- followed by exposure to xanthine oxidase for 5 minutes
Results and discussion
Effect levels
- Sex:
- male
- Remarks on result:
- other: hydrogen peroxide and hydroxyl radical converted from superoxide anion caused an intense airway inflammation.
Any other information on results incl. tables
Inhalation of xanthine/xanthine oxidase produced a marked Pontamine sky blue exudation in the trachea, main bronchus and lungs. The xanthine/xanthine oxidase-induced increase in Pontamine sky-blue exudation was attenuated by pretreatment with inhaled catalase, but not by superoxide dismutase. Additionally, in the bronchus and lungs, the increase in Pontamine sky-blue exudation was significantly suppressed by deferoxamine. These results indicate that hydrogen peroxide and hydroxyl radical converted from superoxide anion cause an intense airway inflammation.
Applicant's summary and conclusion
- Interpretation of results:
- study cannot be used for classification
- Conclusions:
- The inhalation of xanthine for 5 minutes followed by inhalation of xanthine oxidase for 5 minutes, indicates that hydrogen peroxide and hydroxyl radical converted from superoxide anion cause an intense airway inflammation.
- Executive summary:
An investigation was run to see if aerosolized xanthine/xanthine oxidase induces airway inflammation in anesthetized guinea pigs. Inhalation of xanthine for 5 min followed by inhalation of xanthine oxidase for 5 min was performed with an ultrasonic nebulizer in anesthetized animals. Airway inflammation was assessed by airway vascular permeability using Pontamine sky blue. Inhalation of xanthine/xanthine oxidase produced a marked Pontamine sky blue exudation in the trachea, main bronchus and lungs. The xanthine/xanthine oxidase-induced increase in Pontamine sky-blue exudation was attenuated by pretreatment with inhaled catalase, but not by superoxide dismutase. Additionally, in the bronchus and lungs, the increase in Pontamine sky-blue exudation was significantly suppressed by deferoxamine. These results indicate that hydrogen peroxide and hydroxyl radical converted from superoxide anion cause an intense airway inflammation.
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