Adrenaline (via α1B-adrenoceptors) and ethanol stimulate OH• radical production in isolated rat hepatocytes

被引：11

作者：

Castrejón-Sosa, M

Villalobos-Molina, R

Guinzberg, R

Piña, E

机构：

[1] Natl Autonomous Univ Mexico, Sch Med, Dept Biochem, Mexico City 04510, DF, Mexico

[2] Natl Polytech Inst, Ctr Res & Adv Studies, Dept Pharmacobiol, Mexico City, DF, Mexico

来源：

LIFE SCIENCES | 2002年 / 71卷 / 21期

关键词：

ethanol; adrenaline; alpha(1B)-adrenoceptors; hepatocytes; hydroxyl radicals;

D O I：

10.1016/S0024-3205(02)02041-6

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Adrenaline is able to increase the oxidative damage caused by some xenobiotic agents in the liver. Ethanol produces oxidative changes in hepatic tissue, while an acute intoxication with alcohol increases adrenaline blood levels. The aim of this study was to determine whether adrenaline increases ethanol-induced hydroxyl free radical production in isolated hepatocytes. Adrenaline augmented hydroxyl radicals in a concentration-dependent manner and was blocked by chloroethylclonidine, an alpha(1B)-adrenoceptor antagonist, while adrenaline plus ethanol added their individual effects. It is suggested that adrenaline increases hydroxyl radicals by an alpha(1B)-adrenoceptor-mediated mechanism, while ethanol does so by a receptor-independent mechanism. (C) 2002 Published by Elsevier Science Inc.

引用

页码：2469 / 2474

页数：6

共 19 条

[1] LYMPHOCYTE SPECIFIC HETEROGENEITY IN THE RAT LEUKOCYTE COMMON ANTIGEN (T200) IS DUE TO DIFFERENCES IN POLYPEPTIDE SEQUENCES NEAR THE NH2-TERMINUS [J].