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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
Carcinogenicity
Administrative data
- Endpoint:
- carcinogenicity, other
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- study well documented, meets generally accepted scientific principles, acceptable for assessment
Data source
Reference
- Reference Type:
- publication
- Title:
- Comparative Inhibiting Effects of Methylxanthines on Urethan-induced Tumors, Malformations, and Presumed Somatic Mutations in Mice
- Author:
- Nomura T
- Year:
- 1 983
- Bibliographic source:
- Cancer Research, 43:1342-1346
Materials and methods
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- Methylxanthines were given i.p. at 6-hr intervals during a period of 0 to 24 hours after urethan.
- GLP compliance:
- not specified
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:
- mouse
- Strain:
- other: ICR/Jc1, PT, or HT
- Remarks:
- Jc1
Administration / exposure
- Route of administration:
- intraperitoneal
- Duration of treatment / exposure:
- 0-36 hours
- Frequency of treatment:
- 7 i.p. injections given at 6 hour intervals 0-36 hours after urethan treatment
Doses / concentrations
- Dose / conc.:
- 0.38 other: %
Results and discussion
Effect levels
- Remarks on result:
- other: No significant increase was observed in lung tumors in tumor-bearing mice when 0.38% was given i.p. after urethan treatment.
Applicant's summary and conclusion
- Conclusions:
- No significant increase was observed in lung tumors in tumor-bearing mice when 0.38% was given i.p. after urethan treatment.
- Executive summary:
The inhibiting effects of methylxanthines on urethan-induced lung tumors, malformations, and presumed somatic mutations in mice were studied to determine the contribution of mutational and physiological changes to chemically induced neoplasia and malformation. When young adult or pregnant ICR/Jc1 mice were treated with urethan and then methylxanthines were given, caffeine (1,3,7-trimethylxanthine) and theobromine (3,7-dimethylxanthine) greatly suppressed urethan-induced tumorigenesis and teratogenesis, while the theophylline (1,3-dime-thylxanthine) did not. Of the three monomethylxanthines (methylated at positions 1, 3, or 7), 7-methylxanthine was most effective for inhibiting tumors and malformations, indicating that the methyl group at position 7 is most active. Contribution of cyclic adenosine 3': 5' monophosphate was ruled out, since urethan-induced tumorigenesis and teratogenesis were not affected by the theophylline which elevates the cellular level of cyclic adenosine 3':5'-monophosphate by inhibiting phosphodiesterase more effectively than caffeine does; instead, tumorigenesis and teratogenesis were greatly inhibited by the theobromine and 7-methylxanthine,which do not alter the level of cyclic adenosine 3':5'-monophosphate.To test the mutational origin of cancer and malformation ,the effects of caffeine on urethan induction of somatic mutations in PTXHTF-, mice were examined, because caffeine is known to inhibit ultraviolet and 4-nitroquinoline 1-oxide-initiated mutagenesis in Escherichia coli by inhibiting error-prone repair. In mice, however, caffeine did not inhibit urethan induced somatic mutations. Furthermore, theophylline, an inhibitor of error-prone repair, did not reduce the yields of tumors and malformations. Anti-neoplastic and antiteratogenic effects of caffeine may be caused not by the inhibition of the mutational change but by the inhibition of the subsequent process for expressing tumors and malformations.
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