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Toxicological information

Basic toxicokinetics

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Administrative data

Endpoint:
basic toxicokinetics in vivo
Type of information:
experimental study
Adequacy of study:
weight of evidence
Reliability:
4 (not assignable)
Rationale for reliability incl. deficiencies:
secondary literature

Data source

Reference
Reference Type:
secondary source
Title:
cited in Final Report on the Safety Assessment of Triethylene Glycol and PEG-4 (2006).
Author:
McKennis et al.
Year:
1962
Bibliographic source:
International Journal of Toxicology 25 (2), 121 - 138

Materials and methods

Objective of study:
absorption
distribution
excretion
metabolism
Principles of method if other than guideline:
no information available about testing method
GLP compliance:
no

Test material

Reference
Name:
Unnamed
Type:
Constituent
Test material form:
liquid
Radiolabelling:
no

Test animals

Species:
rabbit
Strain:
New Zealand White
Sex:
female
Details on test animals and environmental conditions:
no data

Administration / exposure

Route of administration:
oral: gavage
Vehicle:
not specified
Details on exposure:
2 female rabbits were given single doses of 200 or 2000 mg/kg TEG on stomach tube. Urine from the dosed animals was subsequently collected for 24 hours.
Duration and frequency of treatment / exposure:
24 hours
Doses / concentrationsopen allclose all
Dose / conc.:
200 mg/kg bw (total dose)
Remarks:
Low dose rabbits
Dose / conc.:
2 000 mg/kg bw (total dose)
Remarks:
High dose rabbits
No. of animals per sex per dose:
2 female rabbits
Control animals:
not specified

Results and discussion

Any other information on results incl. tables

Rabbits dosed with 200 or 2000 mg/kg TEG respectively excreted 34.3% or 28% of the dose amount as unchanged TEG. The urine of 1 rabbit contamined 35.2% of the administered dose as a hydroxyacid form of TEG.

Applicant's summary and conclusion

Conclusions:
Interpretation of results: In discussing treatment of TEG poisoning, it was stated that TEG is believed to be metabolized in mammals by alcohol dehydrogenase to acidic products causing metabolic acidosis. TEG metabolism by alcohol dehydrogenase can be inhibited by 4-methyl pyrazole. In discussing treatment of TEG poisoning, it was stated that TEG is believed to be metabolized in mammals by alcohol dehydrogenase to acidic products causing metabolic acidosis. TEG metabolism by alcohol dehydrogenase can be inhibited by 4-methyl pyrazole or ethanol.