绿豆线粒体呼吸链在不同电子传递途径中的电子漏

绿豆线粒体的呼喊链在氧化不同义莪时有不同的呼吸速率和电子漏速率,但是Ｏ２＾－／Ｏ２比值较稳定。呼吸链部位Ⅱ的抑制剂抗霉素Ａ对α－酮茂二酸、琥珀酸及苹果本工物时的电子漏速率和Ｏ２＾－／Ｏ２比值都明显的促进作用,说明电子漏发生的位点可能在抗纱Ａ的抑制点之前。呼吸链在氧化外源ＮＡＤＨ时,线料体所产生的地氰化物、鱼藤酮、抗弱Ａ及ＳＨＡＭ都不敏感,而对钙离子的螯合剂ＥＧＴＡ显著敏感。因此,依赖于钙离子的ＮＡ     

线粒体呼吸链功能调控机制的研究进展

核基因组与线粒体基因组的相互作用,以及两基因组在调控呼吸链亚基的表达机制方面一直处于探索阶段,线粒体核转录因子的发现,使细胞核调控呼吸链亚基表达的研究得到了很大的发展。本文就近年来对核呼吸因子和细胞核对呼吸链的调控机制研究作一介绍。     

线粒体电子传递链电子漏的化学发光测定

本实验用差速离心法分离正常大鼠肝脏和心肌线粒体 ,以lucigenin (探测超氧阴离子 )与luminol (探测过氧化氢 )为探剂 ,用化学发光法测定METC电子漏的生成。在反应体系中加入外源底物 ,其发光强度明显高于空白对照 (体系中无线粒体 )。在肝线粒体体系中 ,无论是lucigenin还是luminol诱发的发光 ,琥珀酸底物引起的发光强均要高于丙酮酸 /苹果酸引起的发光强度。在心肌线粒体 luminol体系中也有与肝线粒体相似的结果 ,在心肌线粒体 lucigenin体系中 ,加入外源底物丙酮酸 /苹果酸诱发的发光强度高于琥珀酸诱发的发光强度     

线粒体结构和功能改变对阿尔茨海默病发生的影响

阿尔茨海默病(Alzheimer's disease,AD)是一种以进行性认知障碍和行为损害为主要特征的神经退行性疾病,主要临床表现为认知功能障碍,同时伴发精神障碍和情绪障碍.AD患者脑中早期即表现出细胞内线粒体功能紊乱和结构变化,纠正线粒体稳态失衡及由其引起的细胞病理改变可能是早期治疗AD的潜在靶点.该文主要对线粒体...     

水生动物和大鼠线粒体的呼吸链比较

用陆生哺乳动物线粒体呼吸链与水生动物线粒体呼吸链相比较的研究方法,探讨了呼吸链的功能与环境相适应的关系。研究了淡水中生活的草鱼肝丝线粒体,观察到琥珀酸脱氢酶的活性非常低,而ＮＡＤＨ脱氢酶和泛醌细胞色素Ｃ还原酶的活性较高。但海洋生物海绵的线粒体ＮＡＤＨ脱氢酶和琥垢酸脱氢酶的活性都非常低。     

线粒体呼吸链复合体Ⅱ＋Ⅲ的电子传递与质子转移的偶联

研究了鼠肝线粒体内膜体呼吸链复合体Ⅱ＋Ⅲ的Ｈ＾＋／２ｅ比与△ψ的相关性及其调节因素,证明：（１）用光谱法测得复合体Ⅱ＋Ⅲ的电子传递与质子转换初速度的Ｈ＾＋／２ｅ比值接近４,与铁氰化钾脉冲法测得的结果相同,Ｈ＾＋／２ｅ随着△μＨ＾＋升高而逐渐下降,荧光透析法测定不同Ｆｅ＾３＋还原速率建立的不同△ψ时,证明Ｈ＾＋回漏对△ψ和Ｈ＾＋泵出速度的依赖性,讨论了呼吸链复合体Ⅱ＋Ⅲ电子传递与质子转移之间的偶联以     

疲劳性运动中线粒体电子漏引起质子漏增加

以大鼠递增强度力竭性竭性跑台运动为疲劳运动模型,观察了运动后大鼠骨骼肌线粒体电子漏和质子漏的变化。结果表明,运动性疲劳状态下大鼠骨骼肌线粒体超氧阴离子生成增加,脂质过氧线粒体质子漏增多是氧化磷酸化偶联程度下降的重要因素。实验结果支持电子漏引起质子漏的假说。     

线粒体蛋白质组学研究进展

线粒体是真核生物中重要的细胞器,其包含的全部蛋白质称为线粒体蛋白质组。人类线粒体大约包含1500多种蛋白质,由核基因和线粒体基因共同编码。线粒体是细胞能量合成和物质代谢的中心,其功能障碍将直接或问接引起许多疾病。目前线粒体蛋白质组学正是系统性地研究线粒体在生理、病理过程中的功能变化以及研究疾病发生机制的重要方法。将线粒体蛋白质组的研究方法、研究进展、线粒体蛋白质组的性质及其在相关疾病研究中的作用进行综述,并对线粒体蛋白质组学在疾病发生机制和诊断治疗中的发展前景进行展望。     

线粒体呼吸链复合体Ⅰ

线粒体呼吸链复合体Ⅰ（简称复合体Ⅰ）是呼吸链电子传递的起始复合体,作为电子传递过程的限速酶,复合体Ⅰ的分子量远大于其余的四个呼吸链复合体。复合体Ⅰ相关的疾病发生除了与40余个复合体Ⅰ组成亚基的突变相关外,还同参与其组装的多个组装因子存在密切联系。该文对复合体I的结构以及参与调控复合体Ⅰ组装的各类组装因子进行了综述,旨在为全面了解复合体Ⅰ相关疾病的发生提供具体参考。     

低温胁迫下植物线粒体膜与抗氰呼吸的关系

主要论述了植物处于低温胁迫下其线粒体膜脂与膜蛋白的变化以及在低温伤害反应中植物所产生的活性氧对抗氰呼吸的影响。     

线粒体，活性氧和细胞凋亡

在能量代谢和自由基代谢中,线粒体均占据着十分重要的地位.通过呼吸链电子漏途径,线粒体产生大量超氧阴离子,并通过链式反应形成对机体有损伤作用的活性氧.通过呼吸链电子漏,氧化磷酸化解偶联,线粒体内膜产生通透性转变孔道（PTP）及Box-和/或PTP-介导的细胞色素c向胞质的转移等种种因素,线粒体参与一般抗氧化防御及细胞凋亡等重要生理过程的调控.在与线粒体相关的细胞凋亡中,活性氧的信号作用是十分明显的.     

呼吸链电子漏在细胞凋亡中的作用

实验证明细胞色素c具有很强的抗氧化功能,在线粒体中氧化态的细胞色素c直接清除O2·-,还原态的细胞色素c清除H2O2.由于呼吸链传递电子合成ATP的同时,总有少部分电子从呼吸链底物端的复合物Ⅰ和Ⅲ漏出,而且漏出的电子首先使氧分子还原成O2·- ,然后O2·-歧化成H2O2,所以细胞色素c清除O2·-和H2O2的功能使呼吸链出现了两条电子漏旁路.细胞色素c通过这两条电子漏路径实现其控制线粒体中O2·-和H2O2水平的功能.根据两条电子漏旁路都是O2·-代谢路径的事实,引进了线粒体自由基代谢的概念,并从自由基代谢失调的角度探讨了呼吸链电子漏在细胞凋亡中的作用.     

脱落酸对玉米胚芽和大豆子叶线粒体呼吸的影响

在提取玉米和大豆线粒体后,以ABA处理线粒体,发现在不同底物存在下,ABA均可增加线粒体的耗氧速率,呼吸速率随ABA浓度变化的结合常数（Kd）值为1．43μmol／L。ABA对4态呼吸的促进作用更为显著,因而导致呼吸控制下降,P／O比降低。蛋白质合成抑制剂环己酰亚胺不影响ABA的效应。以ABA预处理大豆子叶,虽然也促进了呼吸作用,但不改变呼吸控制和P／O.     

Mechanism of Superoxide Anion Generation in Intact Mitochondria in the Presence of Lucigenin and Cyanide

In the presence of cyanide and various respiratory substrates (succinate or pyruvate + malate) addition of high concentrations of lucigenin (400 microM; Luc2+) to rat liver mitochondria can induce a short-term flash of high amplitude lucigenin-dependent chemiluminescence (LDCL). Under conditions of cytochrome oxidase inhibition by cyanide the lucigenin-induced cyanide-resistant respiration (with succinate as substrate) was not inhibited by uncouplers (FCCP) and oligomycin. Increase in transmembrane potential (Deltaphi) value by stimulating F0F1-ATPase functioning (induced by addition of MgATP to the incubation medium) caused potent stimulation of the rate of cyanide-resistant respiration. At high Deltaphi values (in the presence of MgATP) cyanide resistant respiration of mitochondria in the presence of succinate or malate with pyruvate was insensitive to tenoyltrifluoroacetone (TTFA) or rotenone, respectively. However, in both cases respiration was effectively inhibited by myxothiazol or antimycin A. Mechanisms responsible for induction of LDCL and cyanide resistant mitochondrial respiration differ. In contrast to cyanide-resistant respiration, generation of LDCL signal, that was suppressed only by combined addition of Complex III inhibitors, antimycin A and myxothiazol, is a strictly potential-dependent process. It is observed only under conditions of high Deltaphi value generated by F0F1-ATPase functioning. The data suggest lucigenin-induced intensive generation of superoxide anion in mitochondria. Based on results of inhibitor analysis of cyanide-resistant respiration and LDCL, a two-stage mechanism of autooxidizable lucigenin cation-radical (Luc*+) formation in the respiratory chain is proposed. The first stage involves two-electron Luc2+ reduction by Complexes I and II. The second stage includes one-electron oxidation of reduced lucigenin (Luc(2e)). Reactions of Luc(2e) oxidation involve coenzyme Q-binding sites of Complex III. This results in formation of autooxidizable Luc*+ and superoxide anion generation. A new scheme for lucigenin-dependent electron pathways is proposed. It includes formation of fully reduced form of lucigenin and two-electron-transferring shunts of the respiratory chain. Lucigenin-induced activation of superoxide anion formation in mitochondria is accompanied by increase in ion permeability of the inner mitochondrial membrane.     

An Overview: The Diversified Role of Mitochondria in Cancer Metabolism

Mitochondria are intracellular organelles involved in energy production, cell metabolism and cell signaling. They are essential not only in the process of ATP synthesis, lipid metabolism and nucleic acid metabolism, but also in tumor development and metastasis. Mutations in mtDNA are commonly found in cancer cells to promote the rewiring of bioenergetics and biosynthesis, various metabolites especially oncometabolites in mitochondria regulate tumor metabolism and progression. And mutation of enzymes in the TCA cycle leads to the unusual accumulation of certain metabolites and oncometabolites. Mitochondria have been demonstrated as the target for cancer treatment. Cancer cells rely on two main energy resources: oxidative phosphorylation (OXPHOS) and glycolysis. By manipulating OXPHOS genes or adjusting the metabolites production in mitochondria, tumor growth can be restrained. For example, enhanced complex I activity increases NAD⁺/NADH to prevent metastasis and progression of cancers. In this review, we discussed mitochondrial function in cancer cell metabolism and specially explored the unique role of mitochondria in cancer stem cells and the tumor microenvironment. Targeting the OXPHOS pathway and mitochondria-related metabolism emerging as a potential therapeutic strategy for various cancers.     

Preparation and Properties of Mitochondria from Naegleria gruberi*

Whole cell respiration rates were measured polarographically for Naegleria gruberi during growth in agitated cultures. Log growth phase amebae consumed 80 ng atoms O/min/mg cell protein. At stationary phase, respiration rate decreased 4–fold. Intact mitochondria were isolated from N. gruberi and their oxidative and phosphorylative capacities were studied polarographically. As with the mammalian system, the mitochondria oxidized succinate and NAD-linked substrates, but unlike rat liver mitochondria, those from the protozoan rapidly oxidized citrate and NADH. The rates of substrate oxidation were ADP-dependent, with ADP:O ratios equalling ? 2.8 for NAD-linked substrates and ? 2.2 for succinate. The respiratory control ratios. 2 to 4 for 11 substrates, were dependent on Pi, Mg²⁺, and serum albumin. Potassium cyanide, azide, malonale, and rotenone inhibited electron transport the same way as that of the mammalian system: however, amytal inhibited both glutamate and succinate respiration. Pentachlorophenol, DNP, and bilirubin uncoupled oxidation from phosphorylation. Difference spectra of oxidized and dithionite-reduced mitochondria had distinct absorption bands of flavins and of c-, b-, and α-type cytochromes.     

Reactive Oxygen Species Scavenging Enzymes and Down-Adjustment of Metabolism Level in Mitochondria Associated with Desiccation-Tolerance Acquisition of Maize Embryo

It is a well-known fact that a mature seed can survive losing most of its water, yet how seeds acquire desiccation-tolerance is not well understood. Through sampling maize embryos of different developmental stages and comparatively studying the integrity, oxygen consumption rate and activities of antioxidant enzymes in the mitochondria, the main origin site of reactive oxygen species (ROS) production in seed cells, we found that before an embryo achieves desiccation-tolerance, its mitochondria shows a more active metabolism, and might produce more ROS and therefore need a more effective ROS scavenging system. However, embryo dehydration in this developmental stage declined the activities of most main antioxidant enzymes and accumulated thiobarbituric acid-reactive products in mitochondria, and then destroyed the structure and functional integrity of mitochondria. In physiologically-matured embryos (dehydration-tolerant), mitochondria showed lower metabolism levels, and no decline in ROS scavenging enzyme activities and less accumulation of thiobarbituric acid-reactive products after embryo dehydration. These data indicate that seed desiccation-tolerance acquisition might be associated with down-adjustment of the metabolism level in the late development stage, resulting in less ROS production, and ROS scavenging enzymes becoming desiccation-tolerant and then ensuring the structure and functional integrity of mitochondria.     

Reactive Oxygen Species Scavenging Enzymes and Down-Adjustment of Metabolism Level in Mitochondria Associated with Desiccation-Tolerance Acquisition of Maize Embryo

It is a well-known fact that a mature seed can survive losing most of its water, yet how seeds acquire desiccation- tolerance is not well understood. Through sampling maize embryos of different developmental stages and comparatively studying the integrity, oxygen consumption rate and activities of antioxidant enzymes in the mitochondria, the main origin site of reactive oxygen species （ROS） production in seed cells, we found that before an embryo achieves desiccation-tolerance, its mitochondria shows a more active metabolism, and might produce more ROS and therefore need a more effective ROS scavenging system. However, embryo dehydration in this developmental stage declined the activities of most main antioxidant enzymes and accumulated thiobarbituric acid-reactive products in mitochondria, and then destroyed the structure and functional integrity of mitochondria. In physiologically-matured embryos （dehydration- tolerant）, mitochondria showed lower metabolism levels, and no decline in ROS scavenging enzyme activities and less accumulation of thiobarbituric acid-reactive products after embryo dehydration. These data indicate that seed desiccation- tolerance acquisition might be associated with down-adjustment of the metabolism level in the late development stage, resulting in less ROS production, and ROS scavenging enzymes becoming desiccation-tolerant and then ensuring the structure and functional integrity of mitochondria.     

The Mitochondria of Pre-Erythrocytic Plasmodium berghei

Considerable sectioning was required to demonstrate the mitochondrial cristae of pre-erythrocytic Plasmodium berghei in rat liver. The cristae vary from thin, budding tubules to dilated cisternae and most are obliquely and tangentially sectioned. These factors give the impression of an unusually small number of cristae. Numerous variations of fixation protocols failed to alter significantly the appearance of pre-erythrocytic parasite membranes. The data confirm previous suppositions that certain cytoplasmic bodies noted in pre-erythrocytic mammalian malarial parasites are indeed mitochondria. The term “acristate mitochondria” should be used with great caution in that it raises a serious semantic problem.     

Mitochondria: The hub of energy deprivation-induced autophagy

Macroautophagy/autophagy, a process that is highly conserved from yeast to mammals, delivers unwanted cellular contents to lysosomes or the vacuole for degradation. It has been reported that autophagy is crucial for maintaining glucose homeostasis. However, the mechanism by which energy deprivation induces autophagy is not well established. Recently, we found that Mec1/ATR, originally identified as a sensor of DNA damage, is essential for glucose starvation-induced autophagy. Mec1 is recruited to mitochondria where it is phosphorylated by activated Snf1 in response to glucose starvation. Phosphorylation of Mec1 leads to the assembly of a Snf1-Mec1-Atg1 module on mitochondria, which promotes the association of Atg1 with Atg13. Furthermore, we found that mitochondrial respiration is specifically required for glucose starvation-induced autophagy but not autophagy induced by canonical stimuli. The Snf1-Mec1-Atg1 module is essential for maintaining mitochondrial respiration and regulating glucose starvation-induced autophagy.