HYPOXIA REOXYGENATION ALTERS ENDOTHELIAL PROSTACYCLIN SYNTHESIS - PROTECTION BY SUPEROXIDE-DISMUTASE

被引：25

作者：

PALLUY, O ^{[1
]}

BONNE, C ^{[1
]}

MODAT, G ^{[1
]}

机构：

[1] UNIV MONTPELLIER 1,FAC PHARM,PHYSIOL CELLULAIRE LAB,15 AVE CHARLES FLAHAULT,F-34060 MONTPELLIER,FRANCE

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 1991年 / 11卷 / 03期

关键词：

HYPOXIA REOXYGENATION; ENDOTHELIAL CELLS; FREE RADICAL SCAVENGERS; SUPEROXIDE DISMUTASE; LIPOPEROXIDATION; PROSTACYCLIN SYNTHESIS;

D O I：

10.1016/0891-5849(91)90123-K

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

An in vitor model was designed to study the role of ischemia/reperfusion and oxygen free radicals on vascular prostacyclin (PGI2) synthesis and protection provided by superoxide dismutase (SOD). Cultured bovine aortic endothelial cells (BAEC) were subjected to various times of hypoxia (30 min to 5 h) followed by 30 min reoxygenation. An increase or a decrease in PGI2 synthesis capacity was then observed according to the duration of hypoxia. Inhibition of PGI2 synthesis after 5 h hypoxia/30 min reoxygenation was accompanied by a rise in lipoperoxidation products and a slight cytotoxicity. Superoxide anion could be implicated in these cellular alterations as SOD efficiently prevented these effects. Incubation of normoxic or H/R-treated BAEC with SOD led to an increase in cellular SOD activity as compared to controls. This increase, inhibited by incubation at 4-degrees-C but not by addition of cycloheximide, strongly suggested endocytosis of SOD. This study emphasizes the role of endothelium as a source and target of free radicals and provides a new insight into the mechanism of protection by SOD in ischemia-related vascular pathology.

引用

页码：269 / 275

页数：7

共 39 条

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