Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply

Erich Gnaiger
{"title":"Bioenergetics at low oxygen: dependence of respiration and phosphorylation on oxygen and adenosine diphosphate supply","authors":"Erich Gnaiger","doi":"10.1016/S0034-5687(01)00307-3","DOIUrl":null,"url":null,"abstract":"<div><p>Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome <em>c</em> oxidase. Both perspectives relate to the critical oxygen pressure, which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/P<sub>50</sub>) are reviewed with particular emphasis on the turnover effect under control of adenosine diphosphate ADP concentration, which increases the P<sub>50</sub> in active states. ADP/O<sub>2</sub> flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ADP/O<sub>2</sub> flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing.</p></div>","PeriodicalId":20976,"journal":{"name":"Respiration physiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2001-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0034-5687(01)00307-3","citationCount":"279","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Respiration physiology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0034568701003073","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 279

Abstract

Oxygen limitation is generally considered as impairment of mitochondrial respiration under hypoxia and ischemia. Low intracellular oxygen levels under normoxia, however, imply mild oxygen limitation, provide protection from oxidative stress, and result from economical strategies for oxygen transport through the respiratory cascade to cytochrome c oxidase. Both perspectives relate to the critical oxygen pressure, which inhibits mitochondrial respiration. Based on methodological considerations of oxygen kinetics and a presentation of high-resolution respirometry, mitochondrial oxygen affinities (1/P50) are reviewed with particular emphasis on the turnover effect under control of adenosine diphosphate ADP concentration, which increases the P50 in active states. ADP/O2 flux ratios are high even under severe oxygen limitation, as demonstrated by calorespirometry. Oxygen limitation reduces the uncoupled respiration observed under control by ADP, as shown by relationships derived between ADP/O2 flux ratios, respiratory control ratios, and ADP kinetics. Bioenergetics at low oxygen versus oxidative stress must be considered in the context of limitation of maximum aerobic activity, ischemia-reperfusion injury, mitochondrial signalling to apoptosis, and mitochondrial theories of ageing.

低氧下的生物能量学:呼吸和磷酸化对氧和二磷酸腺苷供应的依赖
氧限制通常被认为是缺氧和缺血情况下线粒体呼吸的损害。然而,在常氧条件下,细胞内低氧水平意味着轻度氧限制,提供氧化应激保护,并且是氧气通过呼吸级联运输到细胞色素c氧化酶的经济策略的结果。这两种观点都与抑制线粒体呼吸的临界氧压有关。基于氧动力学的方法学考虑和高分辨率呼吸测量的介绍,回顾了线粒体氧亲和力(1/P50),特别强调了在二磷酸腺苷ADP浓度控制下的转换效应,这增加了活性状态下的P50。如热肺量测定所示,即使在严重的限氧条件下,ADP/O2通量比也很高。从ADP/O2通量比、呼吸控制率和ADP动力学之间的关系可以看出,氧气限制降低了ADP控制下观察到的非耦合呼吸。低氧与氧化应激下的生物能量学必须在最大有氧活动限制、缺血再灌注损伤、线粒体凋亡信号和线粒体衰老理论的背景下考虑。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信