Registration Dossier

Data platform availability banner - registered substances factsheets

Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Additional toxicological data

Currently viewing:

Administrative data

additional toxicological information
Adequacy of study:
supporting study
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 Type:
Effects of Analogues of Ethanolamine and Choline on Phospholipid Metabolism in Rat Hepatocytes
Bjorn Akesson
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
no guideline followed
GLP compliance:

Test material

Constituent 1
Chemical structure
Reference substance name:
EC Number:
EC Name:
Cas Number:
Molecular formula:

Results and discussion

Applicant's summary and conclusion

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