Paracetamol may cause liver damage by binding covalently and/or by directly or indirectly oxidising nucleophilic sites on cellular macromolecules. Lipid peroxidation has been postulated as a third alternative or additive mechanism. Under some experimental conditions genotoxic effects have also been observed.
Get full access to this article
View all access options for this article.
References
1.
FlaksA., and FlaksB. (1983). Induction of liver cell tumours in IF mice by paracetamol.Carcinogenesis4, 363–368.
2.
DahlinD.C., and NelsonS.D. (1982). Synthesis, decomposition kinetics, and preliminary toxicological studies of pure N-acetyl-p-benzoquinone imine, a proposed toxic metabolite of acetaminophen.Journal of Medical Chemistry25, 885–886.
3.
HolmeJ.A., DahlinD.C., NelsonS.D., and DybingE. (1984). Cytotoxic effects of N-acetyl-p-benzoquinone imine, a common arylating intermediate of paracetamol and N-hydroxy-paracetamol.Biochemical Pharmacology33, 401–406.
4.
HolmeJ.A., and SoderlundE. (1986). Species differences in cytotoxic and genotoxic effects of phenacetin and paracetamol in primary monolayer cultures of hepatocytes.Mutation Research, in press.
5.
DybingE., HolmeJ.A., GordonR., SoderlundE.J., DahlinD.C., and NelsonS.D. (1984). Genotoxicity studies with paracetamol.Mutation Research138, 21–32.
6.
PainterR.B. (1981). DNA synthesis inhibition in mammalian cells as a test for mutagenic carcinogens. In Short-Term Tests for Chemical Carcinogens (ed. SmithH.F., SanR.H.C.), pp. 59–64. New York: Springer-Verlag.
7.
JenssenD. (1984). A quantitative test for mutagenicity in V79 Chinese hamster cells. In Handbook of Mutagenicity Test Procedures (ed. KilbyB.S., LegatorM., NicholsW., RamelC.), pp. 269–290. New York: Elsevier Science Publishers.