Endotoxin inhibits glucuronidation in the liver. An effect mediated by intercellular communication.
Endotoxin [lipopolysaccharide (LPS) 50 micrograms/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.
1st Institute of Biochemistry, Semmelweis University of Medicine, Budapest, Hungary.
G
G
Bánhegyi
I
I
Mucha
T
T
Garzó
F
F
Antoni
J
J
Mandl
D000818:Animals; D002450:Cell Communication / Q000187:drug effects* / Q000502:physiology*; D002478:Cells, Cultured; D003864:Depression, Chemical; D005110:Extracellular Space / Q000502:physiology; D005965:Glucuronates / Q000378:metabolism*; D006019:Glycolysis / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D051379:Mice; D018181:Mice, Inbred CFTR; D009596:Nitrophenols / Q000378:metabolism*; D010477:Perfusion; D011453:Prostaglandins / Q000502:physiology
D005965:Glucuronates; D008070:Lipopolysaccharides; D009596:Nitrophenols; D011453:Prostaglandins; C024836:4-nitrophenol