Transcellular regulation of cell respiration by nitric oxide generated by activated macrophages

被引：60

作者：

Brown, GC

Foxwell, N

Moncada, S

机构：

[1] Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England

[2] UCL, Wolfson Inst Biomed Res, London W1P 9LN, England

来源：

FEBS LETTERS | 1998年 / 439卷 / 03期

基金：

英国惠康基金;

关键词：

nitric oxide; macrophage; mitochondrion; mitochondrial respiration; inflammation; cytotoxicity;

D O I：

10.1016/S0014-5793(98)01404-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

A macrophage cell line (J774), activated with interferon-gamma and endotoxin to express the inducible form of NO synthase (iNOS), immediately inhibited the cellular respiration of co-incubated L-929 fibroblasts or non-activated J774 macrophages, The inhibition was potent, rapid and reversible when the NO was removed by adding oxyhaemoglobin or by inhibiting iNOS. Exogenously added NO also rapidly and reversibly inhibited cellular respiration over the same range of NO concentrations. This inhibition was competitive with oxygen and due to direct inhibition of cytochrome oxidase. Thus, NO generated by one cell can regulate the respiration of adjacent cells, supporting the hypothesis that NO may be a physiological and/or pathological regulator of cellular respiration, via its inhibition of cytochrome oxidase. (C) 1998 Federation of European Biochemical Societies.

引用

页码：321 / 324

页数：4

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