Elsevier

Biochemical Pharmacology

Volume 49, Issue 1, 6 January 1995, Pages 65-68
Biochemical Pharmacology

Research paper
Endotoxin inhibits glucuronidation in the liver: An effect mediated by intercellular communication

https://doi.org/10.1016/0006-2952(94)00389-4Get rights and content

Abstract

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.

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