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 journalArticle

157 Citations (Scopus)

Abstract

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
Volume293
Issue number4
DOIs
StatePublished - Dec 7 1995

Fingerprint

Melatonin
Antioxidants
Lipopolysaccharides
Lipids
Animals
Glutathione Disulfide
Liver
Lipid Peroxidation
Rats
Tissue

Keywords

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

ASJC Scopus subject areas

  • Pollution
  • Pharmacology
  • Toxicology

Cite this

Lipopolysaccharide-induced hepatotoxicity is inhibited by the antioxidant melatonin. / Sewerynek, Ewa; Melchiorri, Daniela; Reiter, Russel J; Ortiz, Genaro G.; Lewinski, Andrzej.

In: European Journal of Pharmacology: Environmental Toxicology and, Vol. 293, No. 4, 07.12.1995, p. 327-334.

Research output: Contribution to journalArticle

Sewerynek, Ewa ; Melchiorri, Daniela ; Reiter, Russel J ; Ortiz, Genaro G. ; Lewinski, Andrzej. / Lipopolysaccharide-induced hepatotoxicity is inhibited by the antioxidant melatonin. In: European Journal of Pharmacology: Environmental Toxicology and. 1995 ; Vol. 293, No. 4. pp. 327-334.
@article{eefe8ca988444865830ea8750e1ba31f,
title = "Lipopolysaccharide-induced hepatotoxicity is inhibited by the antioxidant melatonin",
abstract = "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.",
keywords = "GSH, GSSG, Lipid peroxidant, Lipopolysaccharide, Liver, Melatonin",
author = "Ewa Sewerynek and Daniela Melchiorri and Reiter, {Russel J} and Ortiz, {Genaro G.} and Andrzej Lewinski",
year = "1995",
month = "12",
day = "7",
doi = "10.1016/0926-6917(95)90052-7",
language = "English (US)",
volume = "293",
pages = "327--334",
journal = "Environmental Toxicology and Pharmacology",
issn = "1382-6689",
publisher = "Elsevier",
number = "4",

}

TY - JOUR

T1 - Lipopolysaccharide-induced hepatotoxicity is inhibited by the antioxidant melatonin

AU - Sewerynek, Ewa

AU - Melchiorri, Daniela

AU - Reiter, Russel J

AU - Ortiz, Genaro G.

AU - Lewinski, Andrzej

PY - 1995/12/7

Y1 - 1995/12/7

N2 - 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.

AB - 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.

KW - GSH

KW - GSSG

KW - Lipid peroxidant

KW - Lipopolysaccharide

KW - Liver

KW - Melatonin

UR - http://www.scopus.com/inward/record.url?scp=0028973334&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028973334&partnerID=8YFLogxK

U2 - 10.1016/0926-6917(95)90052-7

DO - 10.1016/0926-6917(95)90052-7

M3 - Article

VL - 293

SP - 327

EP - 334

JO - Environmental Toxicology and Pharmacology

JF - Environmental Toxicology and Pharmacology

SN - 1382-6689

IS - 4

ER -