Pyrrolidine dithiocarbamate protects against thioacetamide-induced fulminant hepatic failure in rats

Rafael Bruck*, Hussein Aeed, Ron Schey, Zipora Matas, Ram Reifen, Gidi Zaiger, Ayala Hochman, Yona Avni

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

70 Scopus citations


Background/Aims: Reactive oxygen species and nuclear factor kappa B (NF-κB) activation have been implicated in the pathogenesis of cell injury in experimental models of liver damage. The aim of the present study was to examine whether pyrrolidine dithiocarbamate (PDTC), an anti oxidant and inhibitor of NF-κB activation, would prevent hepatic damage induced in a rat model of thioacetamide (TAA)-induced liver failure. Methods: Fulminant hepatic failure was induced in the control and treatment groups by two intraperitoneal injections of TAA (either 300 or 400 mg/kg) at 24-h intervals. In the treatment groups, rats were treated also with PDTC (60 mg/kg/24 h, i.p.), initiated 24 h prior to TAA. Results: Liver enzymes, blood ammonia, and hepatic levels of thiobarbituric acid reactive substances (P < 0.001) and protein carbonyls (P < 0.05) were significantly lower in rats treated with PDTC compared to TAA only. Liver histology and the survival rate in the PDTC-treated rats were also improved (P < 0.01 compared to TAA only). NF-κB activation, 2 and 6 h after TAA administration, was inhibited by PDTC. Conclusions: In a rat model of fulminant hepatic failure, the administration of PDTC attenuated liver damage and improved survival. This effect may be due to decreased oxidative stress and inhibition of NF-κB activation.

Original languageAmerican English
Pages (from-to)370-377
Number of pages8
JournalJournal of Hepatology
Issue number3
StatePublished - 2002
Externally publishedYes


  • Fulminant hepatic failure
  • Nuclear factor kappa B
  • Oxidative damage
  • Pyrrolidine dithiocarbamate
  • Reactive oxygen species
  • Thioacetamide


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