Acrylic acid

Neurotoxicity

Administrative data

Endpoint:

neurotoxicity: short-term oral

Type of information:

experimental study

Adequacy of study:

other information

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference

Reference Type:

publication

Title:

Effects of acrylamide and acrylic acid on creatine kinase activity in the rat brain.

Author:

Kohriyama, K. et al.

Year:

1994

Bibliographic source:

Arch. Toxicol., 68, 67-70

Materials and methods

Test guideline

Qualifier:

no guideline available

Principles of method if other than guideline:

Objective: investigation into the biochemical mechanisms of neurotoxicity of acrylamide. Acrylic acid (AA) was examined as an analogue for comparison.
Creatinkinase activity (CK) -considered as a key enzyme in brain metabolism- served as putative indicator for cerebral impairment (correlation between inhibition of CK and regional vulnerability in brain?).

GLP compliance:

not specified

Limit test:

yes

Test material

Test material information

Constituent 1

Reference substance name:

Acrylic acid

EC Number:

201-177-9

EC Name:

Acrylic acid

Cas Number:

79-10-7

Molecular formula:

C3H4O2

IUPAC Name:

prop-2-enoic acid

Details on test material:

no data

Test animals

Species:

rat

Strain:

Wistar

Sex:

male

Administration / exposure

Route of administration:

intraperitoneal

Vehicle:

other: 0.85% NaCI

Analytical verification of doses or concentrations:

yes

Duration of treatment / exposure:

8 d

Frequency of treatment:

on consecutive days

Doses / concentrations

Dose / conc.:

50 mg/kg bw (total dose)

Remarks:

analytical conc.

No. of animals per sex per dose:

7

Control animals:

yes, concurrent vehicle

Details on study design:

Studies were performed in male Wistar rats (7 per group) in vitro and in vivo. In-vivo doses were 8x 50 mg/kg bw administered ip. on consecutive days.
Distribution of test material in the brain was checked separately, using 1-14C-labelled substance. The activity of certain enzymes (i.e. CK, LDH, ASAT) was determined

Results and discussion

Any other information on results incl. tables

Clinical observation: Rats treated with AA did not exhibit any impairment of movement, contrary to those treated with acrylamide (splay of hind limbs and awkward gait), but body weight gain was significantly reduced (> 20 %). Enzyme activities: In vitro AA inhibited CK in dose-related manner, distinctly more pronounced than acrylamide. In vivo, no such inhibition of CK was observed following AA-treatment, but was seen with acrylamide.

This finding seems to correspond to the distinctly higher retention of radioactivity found after ip. infusion of labelled acrylamide than of labelled AA.