REVERSIBLE CONVERSION OF NITROXYL ANION TO NITRIC-OXIDE BY SUPEROXIDE-DISMUTASE

被引：275

作者：

MURPHY, ME ^{[1
]}

SIES, H ^{[1
]}

机构：

[1] UNIV DUSSELDORF,INST PHYSIOL CHEM 1,MOORENSTR 5,W-4000 DUSSELDORF 1,GERMANY

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1991年 / 88卷 / 23期

关键词：

ENDOTHELIUM-DERIVED RELAXING FACTOR; CATALASE; 3-MORPHOLINOSYDNONIMINE HYDROCHLORIDE;

D O I：

10.1073/pnas.88.23.10860

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Superoxide dismutase (SOD) rapidly scavenges superoxide (O2-) and also prolongs the vasorelaxant effects of nitric oxide (NO), thought to be the endothelium-derived relaxing factor. This prolongation has been ascribed to prevention of the reaction between O2- with NO. We report that SOD supports a reversible reduction of NO to NO-. When cyanamide and catalase were used to generate NO- in the presence of SOD, NO was measured by the conversion of HbO2 to MetHb. When SOD[Cu(I)] was exposed to NO anaerobically, NO- was trapped by MetHb forming nitrosylmyoglobin. When NO was generated by 3-morpholinosydnonimine hydrochloride in the presence of SOD, NO- or a similar reductant was formed, which reduced catalase compound II and promoted the formation of the catalase[Fe(III)]-NO complex. It is, therefore, conceivable that SOD may protect NO and endothelium-derived relaxing factor by a mechanism in addition to O2- scavenging and that NO- may be a physiologically important form of endothelium-derived relaxing factor.

引用

页码：10860 / 10864

页数：5

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