Endotoxin inhibits glucuronidation in the liver. An effect mediated by intercellular communication

Gábor Bánhegyi, István Mucha, Tamás Garzó, Ferenc Antoni, József Mandl

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Endotoxin [lipopolysaccharide (LPS) 50 μg/mL] added to the perfusion medium increased glucose production and inhibited the glucuronidation of p-nitrophenol in perfused mouse liver both in recirculating and non-recirculating systems, while sulfation of p-nitrophenol was unchanged. The effects of endotoxin could be prevented by the addition of cyclooxygenase inhibitors, while PGD2 and PGE2 also caused a decrease in p-nitrophenol glucuronidation in perfused liver. In isolated hepatocytes endotoxin failed to affect p-nitrophenol conjugation, while PGD2 and PGE2 decreased the rate of it. Our results suggest that endotoxin inhibits glucuronidation through an intercellular communication presumably mediated by eicosanoids.

Original languageEnglish
Pages (from-to)65-68
Number of pages4
JournalBiochemical Pharmacology
Issue number1
Publication statusPublished - Jan 6 1995



  • eicosanoids
  • endotoxin
  • glucuronidation
  • intercellular communication
  • mouse liver

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology

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