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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Basic toxicokinetics

Currently viewing:

Administrative data

basic toxicokinetics
Type of information:
migrated information: read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
weight of evidence
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: Secondary literature, review

Data source

Reference Type:
review article or handbook
Report date:

Materials and methods

Test material

Constituent 1
Reference substance name:
Automatically generated during migration to IUCLID 6, no data available
Automatically generated during migration to IUCLID 6, no data available
Details on test material:
various alkyl amines

Results and discussion

Any other information on results incl. tables

A.   Excerpt from Cavender et al. 2000:

"In animals, the lower aliphatic amines are mainly metabolized to the corresponding carboxylic acid and urea; the intermediate compounds have been shown by in vitro experiments to be the corresponding aldehyde and ammonia. MAOs oxidatively deaminate primary, secondary, and tertiary amines. However, compounds that have a substituted methyl group on the alpha carbon are not metabolized by MAOs (14).
To serve as a substrate, the amine group must be attached to an unsubstituted methylene group (alpha-carbon hydrogen prerequisite). For example, MAO cannot catalyze the oxidation of aniline, amphetamine, or methylamine. Ethylamine and propylamine have also been demonstrated to be poor substrates for MAO. The rate of enzyme oxidation activity increases with an increase in aliphatic chain length to an optimum of C5 or C6, followed by a decline in activity to a maximum at 13 methylene groups (14a).

For example, butyl-, amyl-, isoamyl-, and heptylamines are readily metabolized to aldehyde and ammonia (15, 16), but compounds of longer chain lengths, for example, octadecylamine, may inhibit the enzyme. Deamination rate also diminishes with secondary and tertiary amines (51a)."

B. Excerpt from Cavender et al. 2000:

"MAO is involved only to a limited extent in the metabolism of aliphatic amines (16), whereas microsomal enzymes can be responsible for multiple amine biotransformations. Microsomal versus mitochrondrial substrate affinity depends not only upon structural characteristics, but also upon the degree of lipophilicity. Microsomal enzyme-catalyzed aliphatic and alicyclic amine biotransformation reactions can include deamination, methylation, N-dealkylation, N-oxidation, N-acetylation, cyclization, N-hydroxylation, and nitrosation (19 - 21)."

C. Excerpt from Cavender et al. 2000:

"In summary, the principal routes of biotransformation of aliphatic and alicyclic amines are N-dealkylation or oxidative deamination and N-oxidation (30a-30b). Primary aliphatic amines are susceptible to N-oxidation only if the alpha-carbon is subtituted. This prevents the formation of a carbinolamine intermediate,and N-oxidation occurs,resulting in formation of primary hydroxylamines, which can then undergo further oxidation to nitroso and oxime metabolites."

Applicant's summary and conclusion