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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Endpoint:
acute toxicity: other routes
Type of information:
experimental study
Adequacy of study:
other information
Reliability:
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: Abstract

Data source

Reference
Reference Type:
publication
Title:
The Effect of Diacetone Alcohol on the Liver of the Rat
Author:
Keith HM
Year:
1931
Bibliographic source:
Proceedings of the Staff Meetings of the Mayo Clinic, 6, 716-717

Materials and methods

Test animals

Species:
rat

Administration / exposure

Route of administration:
intravenous

Results and discussion

Applicant's summary and conclusion

Executive summary:

The hepatotoxic effects of a single large dose ofdiacetone-alcoholwere studied in rats. Rats were given a single, moderately large intravenous injection ofdiacetone-alcohol,and were observed for 5 weeks. Blood and tissue samples were examined at regular intervals for evidence of liver damage. Hemoglobin and erythrocytes were somewhat reduced initially, but returned to normal values by day 6 post injection. Injury to hepatic cells began within 6 hours after treatment, and reached a maximum at about 24 hours, involving all cells in the lobule. Recovery began at 48 hours and was complete at 7 days. Destruction of Kuppfer cells paralleled that of parenchymal cells. Their recovery, however, seemed to proceed from an extraneous source, and their rapid increase continued for 3 or 4 weeks. In many instances, these proliferating histocytes were arranged into nests of cells scattered along the sinusoids, and some nests contained nucleated erythrocytes after day 21. After 5 weeks, livers were entirely normal. The author concludes that the newly formed histocytes in the liver temporarily assumed hemopoietic functions due to an excessive load on the normal hemopoietic centers.