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EC number: 200-076-7 | CAS number: 51-03-6
- 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
Specific investigations: other studies
Administrative data
- Endpoint:
- mechanistic studies
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Study period:
- 1997
- Reliability:
- 1 (reliable without restriction)
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Effect of Piperonyl Butoxide on Cell Replication and Xenobiotic Metabolism in the Livers of CD-1 Mice and F344 Rats
- Author:
- Phillips, J.C., Price, R.J., Morag, E. Cunninghame, M.E., Osimitz, T.G., Cockburn, A., Gabriel, K.L., Preiss, F.J., Butler W.H., Lake, B.G.
- Year:
- 1 997
- Bibliographic source:
- Fund. Appl. Toxicol. 38, 64 - 74.
Materials and methods
- GLP compliance:
- no
- Type of method:
- in vivo
Test material
- Reference substance name:
- 2-(2-butoxyethoxy)ethyl 6-propylpiperonyl ether
- EC Number:
- 200-076-7
- EC Name:
- 2-(2-butoxyethoxy)ethyl 6-propylpiperonyl ether
- Cas Number:
- 51-03-6
- Molecular formula:
- C19H30O5
- IUPAC Name:
- 2-(2-butoxyethoxy)ethyl 6-propylpiperonyl ether
Constituent 1
Test animals
- Species:
- other: mice and rats
- Strain:
- other: CD1 strain mice and F344 rats
Administration / exposure
- Route of administration:
- oral: feed
- Vehicle:
- other: NaPB
- Duration of treatment / exposure:
- 42 days
- Details on study design:
- Type: other: enzyme induction hepatotoxicity
Results and discussion
- Details on results:
- The present data demonstrate that PBO can produce liver enlargement in both the mouse and rat which is associated with hyperplasia, hypertrophy, and induction of xenobiotic metabolising enzymes. At the dose levels employed in this study the hepatic effects of PBO in the mouse were similar to but less marked that those of NaPB. In the rat study, high doses of PBO were toxic. Thus, while the formation of eosinophilic nodules in mouse liver may occur by a mechanism similar to that of NaPB and other nongenotoxic inducers of hepatic xenobiotic metabolism, tumor formation in rats at greater than MTD doses is most likely associated with marked liver enzyme induction in conjiunction with a regenerative hyperplasia resulting from PBO- induced hepatoxicity.
Any other information on results incl. tables
RS-Freetext:
In summary, this data demonstrates that PBO can produce liver enlargement in the
mouse and the rat which is associated with induction of xenobiotic metabolism,
hypertrophy, and hyperplasia. The hepatic effects of Piperonyl Butoxide in the
mouse were similar to but less marked than those produced by sodium phenobarbital
. In the rat high doses of Piperonyl Butoxide were hepatotoxic and resulted in
a marked reduction in body weight. Thus while the reported formation of
eosinophilic nodules in mouse liver by Piperonyl Butoxide may occur by a
mechanism(s) similar to that of NaPB and other nongenotoxic enzyme inducers,
the reported tumor formation in rats at greater than the maximum tolerated dose
is most likely associated with marked enzyme induction in conjunction with a
regenerative hyperplasia resulting from Piperonyl Butoxide-induced hepatotoxicity
Applicant's summary and conclusion
- Conclusions:
- The present data demonstrate that PBO can produce liver enlargement in both the mouse and rat which is associated with hyperplasia, hypertrophy, and induction of xenobiotic metabolising enzymes. At the dose levels employed in this study the hepatic effects of PBO in the mouse were similar to but less marked that those of NaPB. In the rat study, high doses of PBO were toxic. Thus, while the formation of eosinophilic nodules in mouse liver may occur by a mechanism similar to that of NaPB and other nongenotoxic inducers of hepatic xenobiotic metabolism, tumor formation in rats at greater than MTD doses is most likely associated with marked liver enzyme induction in conjiunction with a regenerative hyperplasia resulting from PBO- induced hepatoxicity.
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