Acetone potentiation of 1,1,2-trichloroethane hepatotoxicity

J. R. MacDonald, A Jay Gandolfi, I. G. Sipes

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Acetone potentiation of 1,1,2-trichloroethane (TCEA) hepatotoxicity was found to be strongly dosedependent for both acetone and TCEA. An oral dose of 0.5 ml of acetone/kg was the most effective potentiating pretreatment when administered 16 h prior to TCEA. Surprisingly, higher doses of acetone did not potentiate the hepatotoxicity of TCEA, but may have decreased the severity of this toxicity. Acetone potentiation of hepatotoxicity was most pronounced at or near the hepatotoxic threshold for TCEA. While acetone treatment alone did not affect hepatic glutathione (GSH) stores the most consistent effect produced by acetone pretreatment was a significant potentiation of TCEA-induced depletion of hepatic GSH. These findings suggest that critical doses of acetone may enhance the subsequent hepatotoxicity of TCEA via mechanisms that affect the interaction of TCEA and hepatic GSH stores.

Original languageEnglish (US)
Pages (from-to)57-69
Number of pages13
JournalToxicology Letters
Volume13
Issue number1-2
DOIs
StatePublished - 1982

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Acetone
Liver
1,1,2-trichloroethane
Glutathione
Toxicity

ASJC Scopus subject areas

  • Toxicology
  • Medicine(all)

Cite this

Acetone potentiation of 1,1,2-trichloroethane hepatotoxicity. / MacDonald, J. R.; Gandolfi, A Jay; Sipes, I. G.

In: Toxicology Letters, Vol. 13, No. 1-2, 1982, p. 57-69.

Research output: Contribution to journalArticle

MacDonald, J. R. ; Gandolfi, A Jay ; Sipes, I. G. / Acetone potentiation of 1,1,2-trichloroethane hepatotoxicity. In: Toxicology Letters. 1982 ; Vol. 13, No. 1-2. pp. 57-69.
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