ENDOTOXIN INHIBITS GLUCURONIDATION IN THE LIVER - AN EFFECT MEDIATED BY INTERCELLULAR COMMUNICATION

被引：13

作者：

BANHEGYI, G

MUCHA, I

GARZO, T

ANTONI, F

MANDL, J

机构：

[1] SEMMELWEIS UNIV MED,INST BIOCHEM 1,H-1444 BUDAPEST,HUNGARY

[2] HUNGARIAN ACAD SCI,INST ISOTOPES,BUDAPEST,HUNGARY

来源：

BIOCHEMICAL PHARMACOLOGY | 1995年 / 49卷 / 01期

基金：

匈牙利科学研究基金会;

关键词：

GLUCURONIDATION; ENDOTOXIN; EICOSANOIDS; INTERCELLULAR COMMUNICATION; MOUSE LIVER;

D O I：

10.1016/0006-2952(94)00389-4

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Endotoxin [lipopolysaccharide (LPS) 50 mu g/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 PGD(2) and PGE(2) also caused a decrease in p-nitrophenol glucuronidation in perfused liver. In isolated hepatocytes endotoxin failed to affect p-nitrophenol conjugation, while PGD(2) and PGE(2) decreased the rate of it. Our results suggest that endotoxin inhibits glucuronidation through an intercellular communication presumably mediated by eicosanoids.

引用

页码：65 / 68

页数：4

共 27 条

[1] GLYCOGENOLYSIS - AND NOT GLUCONEOGENESIS - IS THE SOURCE OF UDP-GLUCURONIC ACID FOR GLUCURONIDATION [J].