Registration Dossier

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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Administrative data

other: in vitro
Type of information:
migrated information: read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
supporting study
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Non-GLP, non-guideline study, published in peer reviewed literature, minor restrictions in design and/or reporting but otherwise adequate for assessment

Data source

Reference Type:
Effects of 2-ethylhexanoic acid on the production of reactive oxygen species in human polymorphonuclear leukocytes in vitro
Pennanen SMA, Heiskanen KM, Savolainen KM, Komulainen HK
Bibliographic source:
Toxicology Letters, 117 (2000) 79-84

Materials and methods

Principles of method if other than guideline:
Polymorphonuclear leukocytes (PMNL) were exposed to 2-ethylhexanoic acid (2-EHA) in vitro. Production of reactive oxygen species (ROS) was measured and associated cellular processes were explored.
GLP compliance:
Limit test:

Test material

Constituent 1
Reference substance name:
2-ethylhexanoic acid
EC Number:
EC Name:
2-ethylhexanoic acid
Cas Number:
2-ethylhexanoic acid

Results and discussion

Any other information on results incl. tables

The authors found that 2-EHA:
1) applied at 10-2000 µM did not affect the viability of the cells,
2) did not induce an increase in the production of ROS,
3) inhibited dose dependently the ROS production induced in the PMNL by the cell surface receptor antagonist formyl-methionyl-leucyl-phenylalanine (FMLP),
4) did not affect the levels of free intracellular calcium in the cells, 
5) did not inhibit the baseline activity of protein kinase C (PKC),
6) inhibited dose-dependently the cell ROS production induced by phorbol-myristate acetate (PMA) and suppressed the ROS production due to dioctanoyl-s,n-glycerol (DIC8).

Applicant's summary and conclusion