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.
Bánhegyi
G
G
1st Institute of Biochemistry, Semmelweis University of Medicine, Budapest, Hungary.
Mucha
I
I
Garzó
T
T
Antoni
F
F
Mandl
J
J
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