Interaction of nitric oxide with a functional model of cytochrome c oxidase

被引：40

作者：

Collman, James P. ^{[1
]}

Dey, Abhishek ^{[1
]}

Decreau, Richard A. ^{[1
]}

Yang, Ying ^{[1
]}

Hosseini, Ali ^{[1
]}

Solomon, Edward I. ^{[1
]}

Eberspacher, Todd A. ^{[1
]}

机构：

[1] Stanford Univ, Dept Chem, Stanford, CA 94305 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2008年 / 105卷 / 29期

关键词：

amyl nitrite; cyanide poisoning; synthetic functional model; EPR;

D O I：

10.1073/pnas.0804257105

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：

Cytochrome c oxidase (CcO) is a multimetallic enzyme that carries out the reduction of O-2 to H2O and is essential to respiration, providing the energy that powers all aerobic organisms by generating heat and forming ATP. The oxygen-binding heme a(3) should be subject to fatal inhibition by chemicals that could compete with O-2 binding. Near the CcO active site is another enzyme, NO synthase, which produces the gaseous hormone NO. NO can strongly bind to heme a(3), thus inhibiting respiration. However, this disaster does not occur. Using functional models for the CcO active site, we show how NO inhibition is avoided; in fact, it is found that NO can protect the respiratory enzyme from other inhibitors such as cyanide, a classic poison.

引用

页码：9892 / 9896

页数：5

共 30 条

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[2]

BOWEN WJ, 1949, J BIOL CHEM, V179, P235

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