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EC number: 202-488-2 | CAS number: 96-20-8
- 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
Additional toxicological data
Administrative data
- Endpoint:
- additional toxicological information
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Published data not conforming to a standard guideline but still considered tobe reliable
Data source
Reference
- Reference Type:
- publication
- Title:
- Effects of Analogues of Ethanolamine and Choline on Phospholipid Metabolism in Rat Hepatocytes
- Author:
- Bjorn Akesson
- Year:
- 1 977
- Bibliographic source:
- Biochem. J. (1977) 168, 401-408
Materials and methods
- Type of study / information:
- Study assessing the incorporation of various amino alcohol substances into the phospholipids of isolated rat hepatocytes
Test guideline
- Qualifier:
- no guideline followed
- GLP compliance:
- no
Test material
- Reference substance name:
- 2-aminobutan-1-ol
- EC Number:
- 202-488-2
- EC Name:
- 2-aminobutan-1-ol
- Cas Number:
- 96-20-8
- Molecular formula:
- C4H11NO
- IUPAC Name:
- 2-aminobutan-1-ol
Constituent 1
Results and discussion
Applicant's summary and conclusion
- Conclusions:
- 2-aminobutanol appears to inhibit the incorporation of ethanolamine into phosphatidyl ethanolamine and the incorporation of choline into phosphatidyl choline. 2-amino-2-methylpropanol appeared to inhibit choline incorporation into phosphatidyl choline but not ethanolamine incorporation. This is contrary to other published work (Longmore and Mulford 1962) which dosed in vivo to rats and indicated the contrary effect, i.e. inhibition of ethanolamine incorporation.
- Executive summary:
Analogues of ethanolamine and choline were incubated with different labelled precursors
of phospholipids and isolated hepatocytes and the effects on phospholipid
synthesis were studied. 2. 2-Aminopropan-1-ol and 2-aminobutan-1-ol were the most
efficient inhibitors of ['4C]ethanolamine incorporation into phospholipids, whereas the
incorporation of [3H]choline was inhibited most extensively by NN-diethylethanolamine
and NN-dimethylethanolamine. 3. When the analogues were incubated with [3H]glycerol
and hepatocytes, the appearance of 3H in unnatural phospholipids indicated that they
were incorporated, at least in part, via CDP-derivatives. The distribution of [3H]glycerol
among molecular species of phospholipids containing 2-aminopropan-1-ol and 1-aminopropan-
2-ol was the same as in phosphatidylethanolamine. In other phospholipid analogues
the distribution of 3H was more similar to that in phosphatidylcholine. 4. NNDiethylethanolamine
stimulated both the conversion of phosphatidylethanolamine into
phosphatidylcholine and the incorporation of [Me-14C]methionine into phospholipids.
Other N-alkyl- or NN-dialkyl-ethanolamines also stimulated [14C]methionine incorporation,
but inhibited the conversion of phosphatidylethanolamine into phosphatidylcholine.
This indicates that phosphatidyl-NN-diethylethanolamine is a poor methyl
acceptor, in contrast with other N-alkylated phosphatidylethanolamines. 5. These results
on the regulation of phospholipid metabolism in intact cells are discussed with respect to
the possible control points. They also provide guidelines for future experiments on the
manipulation of phospholipid polar-headgroup composition in primary cultures of
hepatocytes.
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