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右旋糖酐会导致线粒体聚集,并影响其氧化还原酶活性和光散射。

Dextran causes aggregation of mitochondria and influences their oxidoreductase activities and light scattering.

作者信息

Lemeshko Victor V, Solano Sigifredo, López Luis F, Rendón Dairo A, Ghafourifar Pedram, Gómez Luis A

机构信息

Science Department, School of Physics, National University of Colombia, Medellin Branch, AA3840 Medellin, Colombia.

出版信息

Arch Biochem Biophys. 2003 Apr 15;412(2):176-85. doi: 10.1016/s0003-9861(03)00034-1.

DOI:10.1016/s0003-9861(03)00034-1
PMID:12667481
Abstract

It has been reported that dextrans diminish the intermembrane space of mitochondria, increase the number of contact sites between the inner and the outer mitochondrial membranes, decrease the outer membrane permeability to adenosine 5(')-diphosphate, and change the kinetic properties of mitochondrial kinases. In the present work the influence of dextran M40 (5% w/v) on the oxidoreductase activities of the inner and outer membranes of mitochondria, the interaction of cytochrome c with mitochondrial membranes, and the light scattering by rat liver mitochondria were studied. No influence of dextran on the release of cytochrome c from mitochondria or its interaction with mitochondrial membranes was observed. Decreases in the NADH-oxidase (to 80+/-2% of the control), NADH-cytochrome c reductase (to 26+/-2%), succinate-cytochrome c reductase (to 70+/-5%), and NADH-ferricyanide reductase (to 75+/-3%) activities induced by dextran, which may be due to the mitochondrial aggregation, were observed. The formation of aggregates was registered by light scattering, confirmed by light microscopy, and explained within the framework of the Gouy-Chapman theory of the electrical double layer. The observed mitochondrial aggregation seems to be useful also for understanding the mechanisms of mitochondrial condensation and perinuclear clustering during apoptosis.

摘要

据报道,右旋糖酐可减小线粒体的膜间隙,增加线粒体内外膜之间接触位点的数量,降低外膜对腺苷5′-二磷酸的通透性,并改变线粒体激酶的动力学特性。在本研究中,研究了右旋糖酐M40(5% w/v)对线粒体内膜和外膜氧化还原酶活性、细胞色素c与线粒体膜的相互作用以及大鼠肝线粒体光散射的影响。未观察到右旋糖酐对细胞色素c从线粒体释放或其与线粒体膜相互作用的影响。观察到右旋糖酐诱导NADH氧化酶活性(降至对照的80±2%)、NADH-细胞色素c还原酶活性(降至对照的26±2%)、琥珀酸-细胞色素c还原酶活性(降至对照的70±5%)和NADH-铁氰化物还原酶活性(降至对照的75±3%)降低,这可能是由于线粒体聚集所致。通过光散射记录了聚集体的形成,通过光学显微镜证实,并在 Gouy-Chapman 双电层理论框架内进行了解释。观察到的线粒体聚集似乎也有助于理解细胞凋亡过程中线粒体浓缩和核周聚集的机制。

相似文献

1
Dextran causes aggregation of mitochondria and influences their oxidoreductase activities and light scattering.右旋糖酐会导致线粒体聚集,并影响其氧化还原酶活性和光散射。
Arch Biochem Biophys. 2003 Apr 15;412(2):176-85. doi: 10.1016/s0003-9861(03)00034-1.
2
[Interaction of cytochrome c with mitochondrial proteins and cybacrone-dextran].[细胞色素c与线粒体蛋白及环巴胺-葡聚糖的相互作用]
Biokhimiia. 1985 Nov;50(11):1877-83.
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Cytochrome c release from isolated rat liver mitochondria can occur independently of outer-membrane rupture: possible role of contact sites.细胞色素c从分离的大鼠肝脏线粒体中释放可能独立于外膜破裂:接触位点的潜在作用。
Biochem J. 2000 Jun 1;348 Pt 2(Pt 2):343-50.
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Mitochondrial precursor signal peptide induces a unique permeability transition and release of cytochrome c from liver and brain mitochondria.线粒体前体信号肽诱导肝脏和脑线粒体发生独特的通透性转变并释放细胞色素c。
Arch Biochem Biophys. 2001 Feb 15;386(2):251-60. doi: 10.1006/abbi.2000.2201.
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Failure of exogenous NADH and cytochrome c to support energy-dependent swelling of mitochondria.外源性烟酰胺腺嘌呤二核苷酸(NADH)和细胞色素c无法支持线粒体的能量依赖性肿胀。
Arch Biochem Biophys. 2001 Apr 1;388(1):60-6. doi: 10.1006/abbi.2000.2214.
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Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis.缬氨霉素诱导依赖能量的线粒体肿胀、细胞色素 c 释放、细胞质 NADH/细胞色素 c 氧化和细胞凋亡。
Apoptosis. 2011 Oct;16(10):1004-13. doi: 10.1007/s10495-011-0628-7.
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Mg(2+) induces intermembrane electron transport by cytochrome c desorption in mitochondria with the ruptured outer membrane.镁离子通过细胞色素c从外膜破裂的线粒体中解吸来诱导膜间电子传递。
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Membrane potential generation coupled to oxidation of external NADH in liver mitochondria.肝线粒体中与胞外NADH氧化相偶联的膜电位产生
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Hypotonic fragility of outer membrane and activation of external pathway of NADH oxidation in rat liver mitochondria are increased with age.
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Oxidation and reduction of exogenous cytochrome c by the activity of the respiratory chain.通过呼吸链的活性对外源细胞色素c进行氧化和还原。
Arch Biochem Biophys. 1991 Jul;288(1):293-301. doi: 10.1016/0003-9861(91)90198-r.

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