Lipopolysaccharide-induced hepatotoxicity is inhibited by the antioxidant melatonin

Ewa Sewerynek, Daniela Melchiorri, Russel J. Reiter, Genaro G. Ortiz, Andrzej Lewinski

Research output: Contribution to journalArticlepeer-review

160 Scopus citations


Oxidative damage to the liver of lipopolysaccharide-treated rats was evaluated using four parameters: level of lipid peroxidation, changes in total GSH and GSSG concentrations and hepatic morphology. Bacterial lipopolysaccharide (10 mg/kg b.w.) was injected i.p. either at 6, 16 or 24 h before animals were killed. Lipopolysaccharide increased lipid peroxidation most dramatically when it was injected 6 h before killing. Hepatic total GSH increased after lipopolysaccharide in a time-dependent manner. The highest level of GSSG and largest GSSG/total GSH ratio were also observed in the group of animals injected with lipopolysaccharide 6 h before tissue collection. In a second study, lipopolysaccharide was injected 6 h before the animals were killed, with or without 1 mg/kg b.w. melatonin. Melatonin totally abolished lipopolysaccharide-induced increased in lipid peroxidation, exaggerated the rise in total GSH and reversed the increase in GSSG concentration. The liver showed obvious histological degenerative changes after lipopolysaccharide, effects that were counteracted by melatonin administration. The protection conferred by melatonin is presumably due to its antioxidant activity.

Original languageEnglish (US)
Pages (from-to)327-334
Number of pages8
JournalEuropean Journal of Pharmacology: Environmental Toxicology and
Issue number4
StatePublished - Dec 7 1995


  • GSH
  • GSSG
  • Lipid peroxidant
  • Lipopolysaccharide
  • Liver
  • Melatonin

ASJC Scopus subject areas

  • Toxicology
  • Pharmacology
  • Pollution


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