• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

[通过氧化磷酸化系统的酶控制离子通过线粒体膜的转运诱导]

[Control of the induction of ion transport through mitochondrial membranes by the enzymes of the oxidative phosphorylation system].

作者信息

Novgorodov S A, Dragunova S F, Iaguzhinskiĭ L S

出版信息

Biofizika. 1982 Mar-Apr;27(2):244-8.

PMID:6462181
Abstract

It has been shown that the induction of earlier described system of potassium-dependent transport of hydrogen ions in mitochondria at low pH values of the incubation medium is inhibited by the inhibitors of mitochondria respiratory chain and ATPase. It has been found that antimycin and oligomycin suppress the efflux of potassium ions from mitochondria in the presence of succinic acid. The uncoupler (FCCP) turns the effect of ATPase inhibitors to the efflux of potassium ions and acceleration of mitochondria respiration under experimental conditions. At the same time TMPD removes the effect of antimycin on potassium ion efflux from uncoupled FCCP of mitochondria. The data obtained are explained in terms of the postulate that under experimental conditions along with the system of potassium-dependent ion transport there appears leakage of protons through the ATPase channel. A conclusion is made concerning the control of ion transport induction in mitochondria by the enzymes of oxidative phosphorylation system.

摘要

已表明,在孵育介质低pH值条件下,早期描述的线粒体中钾离子依赖性氢离子转运系统的诱导受到线粒体呼吸链抑制剂和ATP酶抑制剂的抑制。已发现,抗霉素和寡霉素在琥珀酸存在下会抑制钾离子从线粒体流出。在实验条件下,解偶联剂(FCCP)会将ATP酶抑制剂的作用转变为钾离子流出并加速线粒体呼吸。同时,TMPD消除了抗霉素对线粒体解偶联FCCP中钾离子流出的影响。根据以下假设对所得数据进行了解释:在实验条件下,除了钾离子依赖性离子转运系统外,质子还会通过ATP酶通道泄漏。得出了关于氧化磷酸化系统的酶对线粒体中离子转运诱导的控制的结论。

相似文献

1
[Control of the induction of ion transport through mitochondrial membranes by the enzymes of the oxidative phosphorylation system].[通过氧化磷酸化系统的酶控制离子通过线粒体膜的转运诱导]
Biofizika. 1982 Mar-Apr;27(2):244-8.
2
[Induction of hydrogen ion transport in mitochondrial membranes].
Biofizika. 1982 Jan-Feb;27(1):52-7.
3
[Mechanism of opiate-induced permeability of mitochondrial membranes for potassium ions].[阿片类药物诱导线粒体膜对钾离子通透性的机制]
Biokhimiia. 1980 Mar;45(3):492-7.
4
[Nucleotide control of ionic transport and ATP synthesis in mitochondria].[线粒体中离子转运和ATP合成的核苷酸调控]
Biokhimiia. 1981 Jul;46(7):1242-8.
5
[Regulation of ion transport in mitochondria by respiratory chain enzymes and ATPase].[呼吸链酶和ATP酶对线粒体离子转运的调节作用]
Biokhimiia. 1984 Feb;49(2):185-92.
6
Ethylazinphos interaction with membrane lipid organization induces increase of proton permeability and impairment of mitochondrial bioenergetic functions.乙嗪磷与膜脂组织的相互作用会导致质子通透性增加以及线粒体生物能量功能受损。
Toxicol Appl Pharmacol. 2001 Sep 15;175(3):209-16. doi: 10.1006/taap.2001.9246.
7
[Effect of tenoyltrifluoroacetone on the functioning of mitochondria and other membrane structures].
Biokhimiia. 1980 Dec;45(12):2165-75.
8
[Respiration toxins as inhibitors of ion transport, supported by ATP hydrolysis, in mitochondria].[作为由线粒体中ATP水解所支持的离子转运抑制剂的呼吸毒素]
Biokhimiia. 1975 Sep-Oct;40(5):934-41.
9
Bax translocation to mitochondria subsequent to a rapid loss of mitochondrial membrane potential.线粒体膜电位迅速丧失后,Bax转位至线粒体。
Cell Death Differ. 2001 Sep;8(9):909-20. doi: 10.1038/sj.cdd.4400889.
10
Indirubin-3'-oxime impairs mitochondrial oxidative phosphorylation and prevents mitochondrial permeability transition induction.靛玉红-3'-肟损害线粒体氧化磷酸化并阻止线粒体通透性转换的诱导。
Toxicol Appl Pharmacol. 2008 Dec 1;233(2):179-85. doi: 10.1016/j.taap.2008.08.005. Epub 2008 Aug 14.

引用本文的文献

1
Ion permeability induction by the SH cross-linking reagents in rat liver mitochondria is inhibited by the free radical scavenger, butylhydroxytoluene.大鼠肝线粒体中SH交联试剂诱导的离子通透性受到自由基清除剂丁基羟基甲苯的抑制。
J Bioenerg Biomembr. 1987 Jun;19(3):191-202. doi: 10.1007/BF00762412.