TY - JOUR. T1 - Electron transport chain of Saccharomyces cerevisiae mitochondria is inhibited by H2O2 at succinate-cytochrome c oxidoreductase level without lipid peroxidation involvement. AU - Cortés-Rojo, Christian. AU - Calderó;n-Cortés, Elizabeth. AU - Clemente-Guerrero, Mónica. AU - Manzo-Ávalos, Salvador. AU - Uribe, Salvador. AU - Boldogh, Istvan. AU - Saavedra-Molina, Alfredo. PY - 2007/11. Y1 - 2007/11. N2 - The deleterious effects of H2O2 on the electron transport chain of yeast mitochondria and on mitochondrial lipid peroxidation were evaluated. Exposure to H2O2 resulted in inhibition of the oxygen consumption in the uncoupled and phosphorylating states to 69% and 65%, respectively. The effect of H2O2 on the respiratory rate was associated with an inhibition of succinate-ubiquinone and succinate-DCIP oxidoreductase activities. Inhibitory effect of H2O2 on respiratory complexes was almost completely recovered by β-mercaptoethanol treatment. H2O2 treatment resulted in full ...

Cloning, Expression and Characterization of Mitochondrial Manganese Superoxide Dismutase from the Whitefly, Bemisia tabaci. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

This page contains the article- A Complex Dietary Supplement Augments Spatial Learning, Brain Mass, and Mitochondrial Electron Transport Chain Activity in Aging Mice http://www.chiro.org/nutrition/ABSTRACTS/A_Complex_Dietary_Supplement_Augments.shtml

Starvation-induced autophagosomes engulf cytosol and/or organelles and deliver them to lysosomes for degradation, thereby resupplying depleted nutrients. Despite advances in understanding the molecular basis of this process, the membrane origin of autophagosomes remains unclear. Here, we demonstrate that, in starved cells, the outer membrane of mitochondria participates in autophagosome biogenesis. The early autophagosomal marker, Atg5, transiently localizes to punctae on mitochondria, followed by the late autophagosomal marker, LC3. The tail-anchor of an outer mitochondrial membrane protein also labels autophagosomes and is sufficient to deliver another outer mitochondrial membrane protein, Fis1, to autophagosomes. The fluorescent lipid NBD-PS (converted to NBD-phosphotidylethanolamine in mitochondria) transfers from mitochondria to autophagosomes. Photobleaching reveals membranes of mitochondria and autophagosomes are transiently shared. Disruption of mitochondria/ER connections by mitofusin2 ...

TY - CHAP. T1 - Isolation and functional assessment of mitochondria from small amounts of mouse brain tissue. AU - Chinopoulos, Christos. AU - Zhang, Steven F.. AU - Thomas, Bobby. AU - Ten, Vadim. AU - Starkov, Anatoly A.. N1 - Copyright: Copyright 2012 Elsevier B.V., All rights reserved.. PY - 2011. Y1 - 2011. N2 - Recent discoveries have brought mitochondria functions in focus of the neuroscience research community and greatly stimulated the demand for approaches to study mitochondria dysfunction in neurodegenerative diseases. Many mouse disease models have been generated, but studying mitochondria isolated from individual mouse brain regions is a challenge because of small amount of the available brain tissue. Conventional techniques for isolation and purification of mitochondria from mouse brain subregions, such as ventral midbrain, hippocampus, or striatum, require pooling brain tissue from six to nine animals for a single mitochondrial preparation. Working with pooled tissue significantly ...

TY - JOUR. T1 - Lipid content, active mitochondria and brilliant cresyl blue staining in bovine oocytes. AU - Casteneda, CA. AU - Kaye, P. AU - Pantaleon, M. AU - Phillips, N. AU - Norman, Scott. AU - Fry, R.. AU - DOcchio, MJ. N1 - Imported on 12 Apr 2017 - DigiTool details were: month (773h) = February, 2013; Journal title (773t) = Theriogenology. ISSNs: 0093-691X; PY - 2013/2. Y1 - 2013/2. N2 - Bovine oocytes that stain with brilliant cresyl blue (BCB) have a relatively higher developmental competence. The aim of the present study was to investigate the relationships among BCB staining, lipid content, and active mitochondria. Bovine oocytes (N = 133) with at least three layers of cumulus cells were segregated as BCB retained (BCB+) or metabolized (BCB-) and then stained for active mitochondria (Mitotracker Red) and lipid (Bodipy), with analysis by confocal microscopy. The BCB+ oocytes (N = 45) contained approximately 26% more cytoplasmic lipid than BCB- oocytes (N = 26-27; P , 0.05). ...

Mitochondria Function, Natural Anti Aging, Health Tips. Whitaker Wellness Institute is Americas largest alternative medicine clinic and wellness center.

RhoA and mitophagy. ​. ​. ​. ​. Dr. Shigeki Miyamoto is directing this project in collaboration with the Brown lab. ​. Mitochondria are essential organelles involved in energy metabolism. Preservation of mitochondrial quality is critical in ensuring cell survival, and even more so in cardiomyocytes which have limited regenerative capacity. Mitochondria damaged in response to stress release reactive oxygen species (ROS) and other toxic molecules which induce cell death. Mitophagy (mitochondria-specific autophagy) eliminates these damaged mitochondria and prevents cell death. Mitophagy is facilitated by mitochondrial fission which segregates damaged mitochondria for elimination. ​. Although there is great interest in developing therapeutic interventions targeting mitochondrial quality control mechanisms to treat ischemic heart disease, intracellular signaling pathways regulating these mitochondrial quality control mechanisms have been elusive and the ideal targets are still unclear. ...

Mitochondrion is one of the most important organelles in cells with several vital responsibilities. The consequence of a deficiency in the function of mitochondrion could result with the wide range of diseases and disorders. In this study, we investigated the feasibility of utilizing surface-enhanced Raman scattering (SERS) to understand the mode of interaction of gold nanoparticles (GNPs) with mitochondria. The living lung cancer cells and the isolated mitochondria from these cells were treated with gold colloidal suspension for SERS experiments. The AFM images of the mitochondria confirmed that the treatment did not cause substantial damage to mitochondria. The localization of GNPs in living cells is investigated with confocal microscopy and found that GNPs form aggregates in the cytosol away from the mitochondria. However, SERS spectra obtained from isolated mitochondria and living cells indicate that GNPs escaped from the endosomes or entered into the living cell through another route may be in

Marta Pera, Delfina Larrea, Cristina Guardia-Laguarta, Jorge Montesinos, Kevin R. Velasco, Rishi R. Agrawal, Yimeng Xu, Robin B. Chan, Gilbert Di Paolo, Mark F. Mehler, Geoffrey S. Perumal, Frank P. Macaluso, Zachary Z. Freyberg, Rebeca Acin-Perez, Jose Antonio Enriquez, Eric A. Schon, Estela Area-Gomez ...

PAYWALLED__T cells with dysfunctional mitochondria induce multimorbidity and premature senescence - posted in BioscienceNews: . P A Y W A L L E D S O U R C E : Science Mag Abstract The impact of immunometabolism on age-associated diseases remains uncertain. Here, we show that T cells with dysfunctional mitochondria due to mitochondrial transcription factor A (TFAM) deficiency act as...

Author(s): Lu, Xiyuan; Kwong, Jennifer Q; Molkentin, Jeffery D; Bers, Donald M | Abstract: Mitochondria produce ATP, especially critical for survival of highly aerobic cells, such as cardiac myocytes. Conversely, opening of mitochondrial high-conductance and long-lasting permeability transition pores (mPTP) causes respiratory uncoupling, mitochondrial injury, and cell death. However, low conductance and transient mPTP openings (tPTP) might limit mitochondrial Ca(2+) load and be cardioprotective, but direct evidence for tPTP in cells is limited.To directly characterize tPTP occurrence during sarcoplasmic reticulum Ca(2+) release in adult cardiac myocytes.Here, we measured tPTP directly as transient drops in mitochondrial [Ca(2+)] ([Ca(2+)]mito) and membrane potential (ΔΨm) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca release, by simultaneous live imaging of 500 to 1000 individual mitochondria. The frequency of tPTPs rose at higher [Ca(2+)]mito, [Ca(2+)]i, with 1 μmol/L peroxide

Our observations in vivo and simulations in silico revealed a novel role of mitochondrial fusion in inheritance. The transport capacity of WT Myo2 obviously is sufficient for the inheritance of a critical quantity of fragmented mitochondria in Δfzo1 cells to sustain viability of most progeny. However, when the transport capacity in myo2(LQ) Δfzo1 cells is compromised, both the number of successful transport events and the mitochondrial mass transported with each event are reduced, leading to a lethal inheritance defect. This can be partially rescued by deletion of the DNM1 gene, which increases the size of individual mitochondria that are transported to the bud with each successful transport event. When bud-directed transport is enforced by expression of Myo2-Fis1 or overexpression of Ypt11, maintenance of a critical mitochondrial size becomes important for retention of mitochondria in the mother. Thus, mitochondria must be in a fused state to ensure partitioning of a critical quantity of ...

Mitochondrial division is important for mitochondrial distribution and function. Recent data have demonstrated that ER-mitochondria contacts mark mitochondrial division sites, but the molecular basis and functions of these contacts are not understood. Here we show that in yeast, the ER-mitochondria tethering complex, ERMES, and the highly conserved Miro GTPase, Gem1, are spatially and functionally linked to ER-associated mitochondrial division. Gem1 acts as a negative regulator of ER-mitochondria contacts, an activity required for the spatial resolution and distribution of newly generated mitochondrial tips following division. Previous data have demonstrated that ERMES localizes with a subset of actively replicating mitochondrial nucleoids. We show that mitochondrial division is spatially linked to nucleoids and that a majority of these nucleoids segregate prior to division, resulting in their distribution into newly generated tips in the mitochondrial network. Thus, we postulate that ...

Great question. Mitochondria are different from the other cellular components in your body. Thats because scientists believe that mitochondria, at one point, were their own independent organisms. They were once bacteria that, somewhere along the way, decided to work together. Because mitochondria evolved doing their own thing, they have their own DNA, and that means they can produce their own proteins and enzymes. Amazing, right?. When your mitochondria are functioning in tip-top shape, they form the foundation for a healthy life, affecting your mood, energy and focus levels, and much, much more. The important takeaway here is that healthy mitochondria provide your body with the steady flow of energy it needs to perform its best in a variety of functions. Its not just the quantity of mitochondria that makes the biggest difference either, its the quality as well.. Because different parts of your body burn massive amounts of energy, when mitochondria production starts to slow, or the quality of ...

Reactive oxygen species (ROS) have been implicated in a wide range of degenerative processes including amyotrophic lateral sclerosis, ischemic heart disease, Alzheimer disease, Parkinson disease and aging. ROS are generated by mitochondria as the toxic by-products of oxidative phosphorylation, their …

Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s). Melatonin protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting the mitochondrial permeability transition pore (MPTP), and activating uncoupling proteins (UCPs). Thus, melatonin maintains the optimal mitochondrial membrane potential and preserves mitochondrial functions. In addition, mitochondrial biogenesis and dynamics is also regulated by melatonin. In most cases, melatonin reduces mitochondrial fission and elevates their

Mitochondria are the major cellular producers of reactive oxygen species (ROS), and mitochondrial ROS production increases steeply with increased proton-motive force. The uncoupling proteins (UCP1, UCP2, and UCP3) and adenine nucleotide translocase induce proton leak in response to exogenously added fatty acids, superoxide, or lipid peroxidation products. Mild uncoupling by these proteins may provide a negative feedback loop to decrease proton-motive force and attenuate ROS production. Using wild-type and Ucp3(-/-) mice, we found that native UCP3 actively lowers the rate of ROS production in isolated energized skeletal muscle mitochondria, in the absence of exogenous activators. The estimated specific activity of UCP3 in lowering ROS production was 90 to 500 times higher than that of the adenine nucleotide translocase. The mild uncoupling hypothesis was tested by measuring whether the effect of UCP3 on ROS production could be mimicked by chemical uncoupling. A chemical uncoupler mimicked the ...

The alternative oxidase of Moniliella tomentosa mitochondria is stimulated by 5-AMP. This effect may be masked, depending on the isolation procedure of the mitochondria. The preparation of submitochondrial particles results in the expression of the 5-AMP effect. Two more methods are now described to reveal the 5-AMP effect whenever it would be masked: (1) switching on the myokinase activity of the mitochondria to deplete them of endogenous 5-AMP; (2) using detergents (sodium dodecyl sulphate, sodium deoxycholate) in a controlled detergent:protein ratio, or chloroform. The alternative oxidase of detergent-solubilized mitochondria was somewhat less selective towards nucleotides than were intact mitochondria. The effect of nucleotides on quinol oxidation by mitochondrial preparations and on quinol autoxidation was also studied. Mitochondrial oxidation of succinate by the alternative oxidase and autoxidation of quinols behaved similarly in the presence of certain nucleotides. Both reactions were ...

Energy production starts at the cellular level with get-up-and-go signals, in the form of ATP, being manufactured in the mitochondria, the powerhouse of your cells. So, when you think energy production, think - mitochondria, more mitochondria, and mitochondrial health. Supplementing with a blend of liposomal glutathione with PQQ and Co-Q10 is one of the best ways to support the powerhouse of your cells, and thereby your energy levels. Glutathione supports the health of the mitochondria by protecting them from oxidative damage or free radical damage (protects the integrity of your DNA too), while Co-Q10 is a necessary electron donor in the energy transport chain, and PQQ (Pyrroloquinoline quinone) is a micronutrient and antioxidant which is involved in enzymatic process that help with energy production of the mitochondria, and encourages mitochondrial biogenesis - the birth of new mitochondria. Kind of makes sense that over time new mitochondria are necessary and…more mitochondria might ...

Two mitochondrial mechanisms have been suggested for the development of pressure overload contractile dysfunction: mitochondrial dysfunction through uncoupling or through reduced oxidative phosphorylation capacity due to PGC-1α downregulation. We assessed the respiratory capacity and coupling to ATP-production, PGC-1α and downstream target gene-expression, as well as fatty acid oxidation and UCP-expression in rat hearts subjected to chronic pressure overload developing heart failure. Transverse aortic constriction for 20 weeks resulted in heart failure with dyspnoea and pleural effusions, decreased ejection fraction (EF: 53±8% vs. 75±6% sham, p,0.05) and LV dilatation (LVEDD 9,9±0,6 vs. 7,6±0,3mm, p,0.05). Mitochondrial respiratory capacity and substrate oxidation rates were significantly affected in failing hearts. State 3 respiration of isolated mitochondria was significantly reduced with all substrates (natomsO/min/mg protein: glutamate 71±16 vs. 361±58, palmitoyl-carnitine 56±4 vs. ...

The function of fatty acid biosynthesis in mitochondria has remained an enigma. In eukaryotic plants, synthesis of fatty acids occurs primarily in plastids such as chloroplasts, and products of this pathway supply acyl precursors for mitochondrial and other extraplastidial membranes. The discovery of ACP in plant mitochondria (4, 5) has raised the possibility that these organelles also participate in de novo fatty acid synthesis. However, ACP has been considered to have several other functions in metabolism, and, in mitochondria, ACP is reported to be one component of the respiratory electron transport chain (14). Thus, whether ACP participates in fatty acid synthesis in plant mitochondria and what function this pathway might have in any eukaryotic organism has been unclear. In this study, we have demonstrated that the de novo synthesis of fatty acids does occur in pea mitochondria, indicating that these organelles possess the complete set of enzymes needed to assemble fatty acids. The analysis ...

The diaminobenzidine (DAB) technique for the ultrastructural localization of sites of cytochrome c oxidase activity in animal tissues has been adapted to the visualization of mitochondria in animal cells growing in culture. The modified technique allows the staining of mitochondria in all cells in coverslip preparatins for light microscopy. Electron microscopy of thin sections of material treated by this method has revealed that all mitochondrial profiles within a cell (and only these) are stained and they exhibit a well preserved size and internal structure. Coverslip cultures of synchronized and unsynchronized HeLa (F-315) cells stained with the DAB reaction were examined under oil immersion. In the majority of the cells, mitochondria were recognized as discrete bodies in the thinner peripheral portion of the cytoplasm. This observation indicates that in a large proportion of HeLa F-315 cells, at least under the growth conditions used here, the mitochondrial complement is dividied into ...

TY - JOUR. T1 - Effects of alcohol and oxidative stress on liver pathology. T2 - The role of the mitochondrion. AU - Cahill, Alan. AU - Cunningham, Carol C.. AU - Adachi, Masayuki. AU - Ishii, Hiromasa. AU - Bailey, Shannon M.. AU - Fromenty, Bernard. AU - Davies, Adrian. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2002. Y1 - 2002. N2 - This article represents the proceedings of a symposium at the 2001 Research Society on Alcoholism meeting in Montreal, Canada. The chairs were Alan Cahill and Carol C. Cunningham. The presentations were (1) Mitochondrial regulation of ethanol-induced hepatocyte apoptosis: possible involvement of proapoptotic Bcl-2 family protein Bax, by Masayuki Adachi and Hiromasa Ishii; (2) Effects of ethanol on mitochondrial reactive oxygen species production and oxidative protein modification, by Shannon M. Bailey; (3) Acute ethanol binges elicit widespread oxidative mitochondrial DNA damage and depletion: protective effects of antioxidants and ...

Fluctuating vs. continuous exposure to H₂O₂: the effects on mitochondrial membrane potential, intracellular calcium, and NF-κB in astroglia.

CPPs (cell-penetrating peptides) facilitate cellular uptake of covalently attached macromolecules, through an as yet controversial mechanism that either involves direct membrane passage or a type of endocytosis. We investigated the potential of the CPPs penetratin and Tat to act as mitochondria-targeting vectors by testing whether they were internalized by isolated mitochondria, and by mitochondria within cells in culture. We also tested peptides conjugated to the mitochondria-targeting moiety triphenylphosphonium. We found no evidence for mitochondrial uptake by penetratin, Tat or their triphenylphosphonium conjugates. This result suggests that CPPs are unsuitable as mitochondria-targeting vectors, and implies an endocytic mode of cellular uptake for CPPs. ...

NEET Biology Mitochondria … 9. NAF‐1, a NEET family protein, promotes Drp1 recruitment to ER‐mitochondria contact sites and induces mitochondrial fragmentation. Plant cells can form all the amino acids. Many vacuoles occur, which are smaller in size. (d) the chloroplasts are generally much larger than mitochondria. introduce tetracycline-inducible expression mitochondrial protein mitoNEET in α- or β-cells as a model of graded mitochondrial dysfunction. The inner mitochondrial membrane has several folds in it called Cristae, so as to increase the surface area. Practice more on a regular basis with these NEET Biology objective questions on air pollution . Mitochondria is tubular in shape. In this issue of Diabetes, Kusminski et al. The 2Fe-2S clusters of NEET proteins were found to be coordinated by a novel 3Cys:1His structure that is relatively labile compared to other 2Fe-2S proteins and is the reason of the NEETs clusters could be transferred to apo-acceptor protein(s) or mitochondria. ...

Fig. 6. Mitotic events of cell division after disruption of mitochondria in the histone EGFP-H1 expressed cell. The disruption of a single mitochondrion by femtosecond laser irradiation had no influence on cell division or cell activity. The cell nuclei and mitotic chromosomes in HeLa cells were visualized using histone EGFP-H1. Mitochondria were stained with MitoTracker Red. Confocal fluorescence image and transmission image (a) before and (b) after femtosecond laser irradiation with 0.39 nJ/pulse (exposure time: 32 ms). The yellow arrow indicates the irradiation point. (c)-(f) Time-lapse confocal images and transmission images. The mitotic events of cell division in the irradiated cells proceeded normally. Scale bar: 20 μm ...

Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8% oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions.

The kinesins form a large family of motor proteins that transport various types of cargo along microtubules. Two members of this family, KIF5 (a kinesin 1) and KIFB1α (a kinesin 3), are known to have roles in mitochondrial transport. Here, Toshihiko Oka and co-workers (p. 2457) identify another kinesin that not only is important for mitochondrial movement but also has a role in regulating mitochondrial morphology. The authors discover this new role for the kinesin-like protein KLP6 - an as yet uncharacterised kinesin 3 - in an RNAi screen for motor proteins involved in mitochondrial morphology in Caenorhabditis elegans. They find that klp6 knockdown results in abnormal mitochondria in the nematode worm. Similarly, the overexpression of rat KLP6 lacking the N-terminal motor domain (which results in dominant-negative effects) causes an increase in short and cup-shaped mitochondria in HeLa cells. In addition, expression of the mutant KLP6 results in slowed anterograde transport in neuronal cells, ...

TY - JOUR. T1 - Intramitochondrial recruitment of endolysosomes mediates Smac degradation and constitutes a novel intrinsic apoptosis antagonizing function of XIAP E3 ligase. AU - Hamacher-Brady, Anne. AU - Choe, S. C.. AU - Krijnse-Locker, J.. AU - Brady, Nathan Ryan. PY - 2014/12/1. Y1 - 2014/12/1. N2 - Intrinsic apoptosis involves BH3-only protein activation of Bax/Bak-mediated mitochondrial outer membrane permeabilization (MOMP). Consequently, cytochrome c is released from the mitochondria to activate caspases, and Smac (second mitochondria-derived activator of caspases) to inhibit XIAP-mediated caspase suppression. Dysfunctional mitochondria can be targeted for lysosomal degradation via autophagy (mitophagy), or directly through mitochondria-derived vesicle transport. However, the extent of autophagy and lysosomal interactions with apoptotic mitochondria remains largely unknown. We describe here a novel pathway of endolysosomal processing of mitochondria, activated in response to canonical ...

Looking for online definition of Chromosome mitochondria (human) in the Medical Dictionary? Chromosome mitochondria (human) explanation free. What is Chromosome mitochondria (human)? Meaning of Chromosome mitochondria (human) medical term. What does Chromosome mitochondria (human) mean?

Abstract: There is great concern with an increase in the number of Americans who are overweight and obese. Fat cells or adipocytes play a central role in obesity. These cells are metabolically active and play a fundamental role in energy allocation and storage. The adipocyte functions as the energy storage cell by storing excess energy in the forms of triglycerides in lipid vesicles within the cell. The morphology of mitochondria is a dynamic process that varies from cell type to cell type and in response to a variety of signals and conditions (Wilson-Fritch, 2002; Wilson-Fritch, 2004). The morphology of mitochondria in the cell often reflects the functions of that type of cell. In my thesis I characterize the changes in mitochondrial morphology and actin during adipogenesis. In this thesis I found that mitochondria undergo a radical change in morphology during the first two days of adipogenesis. In the pre-adipocyte cell mitochondria assume a reticular morphology that is distributed uniformly ...

Back to Science for Kids Plants have both mitochondria and chloroplasts; they can produce their own glucose to fuel cellular respiration. Used under license from Shutterstock.com.) Animal cells, on the other hand, have only mitochondria. Function Worksheets (Opening image copyright by Sebastian Kaulitzki, 2010. This releases . MCQ quiz on Mitochondria multiple choice questions and answers on Mitochondria MCQ questions on Mitochondria objectives questions with answer test pdf for interview preparations, freshers jobs and competitive exams. Web Publishing Information The HTML comments in this page contain the configurationinformation that allows users to edit pages in your web using the Microsoft Web Publishing Wizard or programs which use the Microsoft Web Publishing Wizard such as FrontPad using the same username and password they would use if they were authoring with Microsoft FrontPage. About half in the average cell is in membrane-bound organelles, varying a bit from cell-to-cell. If an ...

Background: Increasing evidence indicates that mitochondrial-derived reactive oxygen species (ROS) and cellular apoptosis contribute to the pathogenesis of cardiac dysfunction. Mitochondrial thioredoxin (Trx2) is a key protein regulating cellular redox and survival, However, but its role in normal cardiac growth has not been determined.. Methods and Results: We have generated cardiac-specific Trx2 knockout mice (Trx2-cKO) to determine the physiological importance of the Trx2 system in the heart. Trx2-cKO mice developed a spontaneous dilated cardiomyopathy at 1 month of age with increased heart size, fibrosis, reduced ventricular wall thickness, and progressive contractile dysfunction, resulting in death due to heart failure by 4 months of age. Cardiac changes in Trx2-cKO mice were accompanied by disruption of mitochondrial integrity and function, as evident by alterations in mitochondrial number, ultrastructure, membrane potential and ATP production. Increases in ASK1 signaling and ROS ...

Researchers find mitochondria could delay aging. A recent study has revealed that mitochondria could be used to combat a universal health issue - aging.. Some in the scientific community are already pushing to have aging classified as a disease worthy of treatment rather than a time of life, and recent findings from a study carried out by Lomonosov Moscow State University and Stockholm University could possibly support this movement. The study examined the role that mitochondria plays in the aging of organisms by treating three groups of mice. The findings, published in Aging, showed the mice that received an artificial antioxidant called SkQ1 aged at a slower rate than those who did not.. About the SkQ1 antioxidant. Russian Professor Vladimir Skulachev created the molecule SkQ1, which contains antioxidants in the cells mitochondria.. Experiments were carried out on three groups of mice - one that had been genetically modified with mutations to age at an accelerated rate from birth, one that ...

article{62f3985e-a946-40ca-a489-6a8f8076cf24, abstract = {,p,Inside-out submitochondrial particles (IO-SMP) were isolated and purified from potato (Solanum tuberosum L. cv.) tubers. When these IO-SMP were incubated with [γ,sup,32,/sup,P]ATP more then 20 proteins became labelled as a result of phosphorylation. The ,sup,32,/sup,P incorporation was stimulated by the oxidizing reagent ferricyanide. Except for a 17 kDa protein which was phosphorylated only in the absence of divalent cations, the protein phosphorylation required Mg,sup,2+,/sup,. The time for half-maximum ,sup,32,/sup,P incorporation was 4 min for the 22 kDa phospho-F,sub,1,/sub, δ-subunit and 2 min for the 28 kDa phospho-F,sub,0,/sub, b-subunit of the proton-ATPase. The K(m) for ATP for the detected phosphoproteins was between 65 μM and 110 μM. The pH optimum for protein phosphorylation in inner membranes was between pH 6 and 8, and for the F,sub,1,/sub, δ-subunit and the F,sub,0,/sub, b-subunit the pH optima were 6.5-8 and pH 8, ...

Mitochondria in oligodendrocyte progenitor cells (OPs) Dtake up and release cytosolic Ca2+ during agonist-evoked Ca2+ waves, but it is not clear whether or how they regulate Ca2+ signaling in OPs. We asked whether mitochondria. play an active role during agonist-evoked Ca2+ release from intracellular stores. Ca2+ puffs, wave initiation, and wave propagation were measured in fluo-4 loaded OP processes using linescan confocal microscopy. Mitochondrial depolarization, measured by tetramethyl rhodamine ethyl ester (TMRE) fluorescence, accompanied Ca2+ puffs and waves. in addition, waves initiated only where mitochondria were localized. To determine whether energized mitochondria were necessary for wave generation, we blocked mitochondrial function with the electron transport chain inhibitor antimycin A (AA) in combination with oligomycin. AA decreased wave speed and puff probability. These effects were not due to global changes in ATP. We found that AA increased cytosolic Ca2+ markedly reduced ...

Increased O(2) metabolism resulting in chronic hypoxia is common in models of endstage renal disease. Mitochondrial uncoupling increases O(2) consumption but the ensuing reduction in mitochondrial membrane potential may limit excessive oxidative stress. The present study addressed the hypothesis that mitochondrial uncoupling regulates mitochondria function and oxidative stress in the diabetic kidney. Isolated mitochondria from kidney cortex of control and streptozotocin-induced diabetic rats were studied before and after siRNA knockdown of uncoupling protein-2 (UCP-2). Diabetes resulted in increased UCP-2 protein expression and UCP-2-mediated uncoupling, but normal mitochondria membrane potential. This uncoupling was inhibited by GDP, which also increased the membrane potential. siRNA reduced UCP-2 protein expression in controls and diabetics (-30-50%), but paradoxically further increased uncoupling and markedly reduced the membrane potential. This siRNA mediated uncoupling was unaffected by GDP ...

New data presented at International Conference on Alzheimers and Parkinsons Diseases. Vancouver, BC - March 12, 2013 - Anavex Life Sciences Corp. (Anavex) (OTCQB: AVXL) today announced more promising new data for ANAVEX 2-73, the companys lead drug candidate for Alzheimers disease.. In a scientific study conducted in France at the University of Montpellier and INSERM, ANAVEX 2-73 demonstrated disease-modifying effects, including the ability to repair normal mitochondrial functionality in the hippocampus, the part of the brain involved with learning, memory and emotions. Mitochondrial dysfunction has been consistently reported as an early cause of Alzheimers disease. It appears before amyloid-beta plaques can start to accumulate and memory loss begins in Alzheimers patients and transgenic mice. In the same study, ANAVEX 2-73 blocked apoptosis (cell death) and oxidative stress, which is believed to prevent the onset of Alzheimers disease.. ANAVEX 2-73 appears to be a valuable drug for ...

The mitochondrial cytochrome c oxidase (complex IV; COX) of the respiratory chain transfers electrons from cytochrome c to oxygen. The activity of the respiratory chain complexes generates a proton-gradient across the inner membrane, which is used by the ATP-synthase to produce ATP for cellular metabolism. In baker´s yeast Saccharomyces cerevisiae complex IV forms a supercomplex with cytochrome c reductase (complex III, bc1) and consists of eight nuclear-encoded and three mitochondrially-encoded subunits. The formation of complex IV is crucial for respiratory growth. The translocase of the outer membrane (TOM complex) imports precursors of nuclear-encoded COX subunits into mitochondria. Subsequently, the presequence translocase (TIM23 complex) transports the majority of these precursor proteins into or across the inner membrane in a membrane potential dependent manner. The presequence translocase-associated motor (PAM) drives the translocation into the mitochondrial matrix. The ATPase activity ...

Perturbations in the regulation of glucose and lipid metabolism are both involved in the insulin resistance in skeletal muscle in obesity and type 2 diabetes (2,3). Previously, our laboratory (30) as well as others (31) have observed that the severity of skeletal muscle insulin resistance in type 2 diabetes and obesity is related to diminished activity of oxidative enzymes. In addition, accumulation of triglycerides in skeletal muscle is also correlated with the severity of insulin resistance and with diminished oxidative enzyme activity in these disorders (23). These observations led therefore to the hypothesis of the current investigation, which is that a functional impairment of mitochondria might contribute to the pathogenesis of insulin resistance in skeletal muscle.. Skeletal muscle is a tissue richly endowed with mitochondria and strongly reliant on oxidative phosphorylation for energy production. To test our hypothesis, we assessed the size and morphology of skeletal muscle mitochondria ...

Perturbations in the regulation of glucose and lipid metabolism are both involved in the insulin resistance in skeletal muscle in obesity and type 2 diabetes (2,3). Previously, our laboratory (30) as well as others (31) have observed that the severity of skeletal muscle insulin resistance in type 2 diabetes and obesity is related to diminished activity of oxidative enzymes. In addition, accumulation of triglycerides in skeletal muscle is also correlated with the severity of insulin resistance and with diminished oxidative enzyme activity in these disorders (23). These observations led therefore to the hypothesis of the current investigation, which is that a functional impairment of mitochondria might contribute to the pathogenesis of insulin resistance in skeletal muscle.. Skeletal muscle is a tissue richly endowed with mitochondria and strongly reliant on oxidative phosphorylation for energy production. To test our hypothesis, we assessed the size and morphology of skeletal muscle mitochondria ...

July 2019. Structural and functional studies reported this month in the journal Nature reveal the molecular basis of remodelling of the inner mitochondrial membrane by the protein complex Mgm1. Mitochondria are the powerhouses of our cells and play a fundamental role in human health. Balanced fusion and fission are essential for the proper function and physiology of these important organelles.. Mitochondria possess two membranes. In humans and animals remodelling of the inner mitochondrial membrane is mediated by a protein complex called OPA1. The related protein complex Mgm1 takes on this role in yeasts and other fungi. Both Mgm1 and OPA1 exist in mitochondria in two forms: a membrane-integrated long form and a short form that is soluble in the intermembrane space. Mutations in the OPA1 gene in humans are a common cause of autosomal dominant optic atrophy-a genetic disorder that affects the optic nerve. Mammalian cells that lack OPA1 and yeast strains that express temperature-sensitive versions ...

The distribution of TPP in cytoplasm fractions of rat liver is studied. When the homogenate was prepared with 0.25M sucrose, about 300% of TPP was present in mitochondria. When the homogenization medium was distilled water, the amount of TPP present in this fraction was markedly decreased, while that present in ... read more the supernatant fluid was increased. Mitochondria suspended in 0.25M sucrose and incubated at 18° C for 10 min release in the suspension fluid about 20% of their TPP; under the same conditions, mitochondria suspended in water release about 65% of their TPP. An increased destruction of TPP was observed as a result of incubation of mitochondria in water at 18° C. The distribution of TPP in fatty liver homogenates prepared in 0.25M sucrose resembles strongly that observed for homogenates of normal rat liver prepared in distilled water; TPP was decreased in the mitochondrial fraction and correspondingly increased in the supernatant. Total TPP is decreased in fatty liver ...

The evolutionary diversity of the HSP70 gene family at the genetic level has generated complex structural variations leading to altered functional specificity and mode of regulation in different cellular compartments. By utilizing Saccharomyces cerevisiae as a model system for better understanding t …

The Marsh-Armstrong lab reports in the July issue of PNAS the suprising discovery that in a location called the optic nerve head, large numbers of mitochondria are shed from neurons to be degraded by the lysosomes of adjoining glial cells. This finding calls into question the assumption that a cell necessarily degrades its own organelles. Davis CH, Kim KY, Bushong EA, Mills EA, Boassa D, Shi T, Kinebuchi M, Phan S, Zhou Y, Bihlmeyer NA, Nguyen JV, Jin Y, Ellisman MH, Marsh-Armstrong. Transcellular degradation of axonal mitochondria PNAS 2014 111 (26) 9633-9638. ...

Here, researchers reported that dysfunctional mitochondria, the cells powerhouses, are associated with defective sperm, contributing to male infertility.

The inner membrane of the mitochondrion folds inwards, forming the cristae. This folding allows a greater amount of membrane to be packed into the mitochondrion. The data in this study demonstrate that subunits e and g of the mitochondrial ATP synthase are involved in generating mitochondrial cristae morphology. These two subunits are non-essential components of ATP synthase and are required for the dimerization and oligomerization of ATP synthase. Mitochondria of yeast cells deficient in either subunits e or g were found to have numerous digitations and onion-like structures that correspond to an uncontrolled biogenesis and/or folding of the inner mitochondrial membrane. The present data show that there is a link between dimerization of the mitochondrial ATP synthase and cristae morphology. A model is proposed of the assembly of ATP synthase dimers, taking into account the oligomerization of the yeast enzyme and earlier data on the ultrastructure of mitochondrial cristae, which suggests that ...

The mitochondrial permeability transition pore (mPTP) plays a critical role in the pathogenesis of cardiovascular diseases, including ischemia/reperfusion injury. Although the pore structure is still unresolved, the mechanism through which cyclophilin D (CypD) regulates mPTP opening is the subject of intensive studies. While post-translational modifications of CypD have been shown to modulate pore opening, specific phosphorylation sites of CypD have not yet been identified. We hypothesized here that phosphorylation of CypD on a serine residue controls mPTP opening and subsequent cell death at reperfusion. We combined in silico analysis with in vitro and genetic manipulations to determine potential CypD phosphorylation sites and their effect on mitochondrial function and cell death. Importantly, we developed an in vivo intramyocardial adenoviral strategy to assess the effect of the CypD phosphorylation event on infarct size. Our results show that although CypD can potentially be phosphorylated at

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Researchers have found that asymptomatic dysfunction of mitochondrial activity in the part of the brain that regulates muscular activity, the cerebellum, may be a first step in the development of Friedreichs ataxia (FA).. A study, Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia that appeared in the journal Disease Models & Mechanisms, suggests early use of targeted therapies that may recover mitochondrial function in FA patients.. FA, a genetic disease characterized by progressive damage to the nervous system, leadA to lack of muscle control. The condition is caused by abnormal expression of the mitochondrial protein frataxin.. Most studies have focused on understanding the role of frataxin in mitochondria activity, and its impact on other mitochondrial proteins - rather than the early molecular steps that trigger FA in the first place.. With that in mind, Dr. David Lynch, a pediatric neurologist at the ...

The manganese superoxide dismutase (MnSOD), located in the mitochondria, is a major antioxidant enzyme that plays an important role in protecting cells from oxidative damage. MnSOD has been suggested to have tumor suppressor function in many cancer types. Surprisingly, the levels of MnSOD in ovarian carcinomas were found elevated compared with normal ovarian epithelium. In this study, we aimed to investigate the levels of MnSOD protein in ovarian cancer cell lines and ovarian surface epithelial (OSE) cells and a possible link between MnSOD expression and resistance to apoptosis. We showed that MnSOD protein was abundant in most ovarian cancer cell lines but was at very low levels in OSE. MnSOD overexpression in ovarian cancer cells caused a ~50% decrease of cell proliferation and an increase of apoptosis, whereas targeted inhibition of endogenous MnSOD using small interfering RNA promoted growth of these cells, confirming the effect was MnSOD specific. Furthermore, stimulation of mitochondrial ...

TY - JOUR. T1 - Influence of insulin status on extra-mitochondrial oxygen metabolism in the rat. AU - Satav, J. G.. AU - Dave, K. R.. AU - Katyare, S. S.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - The effects of alloxan diabetes and subsequent treatment with insulin on extra-mitochondrial oxygen metabolism in terms of D-amino acid oxidase (DAAO), xanthine oxidase and catalase were examined. The DAAO activity in the liver with Dalanine and D-serine decreased by 33-62% in the diabetic group while the decrease in the kidneys was 61-74%. Insulin treatment resulted in overstimulation of DAAO activity in the liver but not in the kidneys. Tissue glycogen content was lowered in the diabetic animals but was restored by insulin treatment. Tissue glycogen content and DAAO activity showed an inverse relationship. The xanthine oxidase activity in the two tissues decreased from 40-55%; the catalase activity decreased from 34-54%. Insulin treatment was unable to restore the xanthine oxidase and catalase activities in ...

1. The respiration rate of rat liver mitochondria was stimulated by up to 70% when the extramitochondrial Ca2+ concentration was raised from 103 to 820 nM. This occurred when pyruvate, 2-oxoglutarate, or threo-(Ds)-isocitrate was employed as substrate, but not when succinate was used. 2. Ruthenium Red prevented the stimulation of mitochondrial respiration by extramitochondrial Ca2+, showing that the effect required Ca2+ uptake into the mitochondrial matrix. 3. Starvation of rats for 48 h abolished the stimulation of mitochondrial respiration by extramitochondrial Ca2+ when pyruvate was used as substrate, but did not affect the stimulation of 2-oxoglutarate oxidation by extramitochondrial Ca2+. 4. Our findings are in accord with proposals that oxidative metabolism in liver mitochondria may be stimulated by Ca2+ activation of intramitochondrial dehydrogenases. ...

Metformin is widely used in the treatment of diabetes, and there is interest in repurposing the drug for cancer prevention or treatment. However, the mechanism underlying the metabolic effects of metformin remains poorly understood. We performed respirometry and stable isotope tracer analyses on cells and isolated mitochondria to investigate the impact of metformin on mitochondrial functions. We show that metformin decreases mitochondrial respiration, causing an increase in the fraction of mitochondrial respiration devoted to uncoupling reactions. Thus, cells treated with metformin become energetically inefficient, and display increased aerobic glycolysis and reduced glucose metabolism through the citric acid cycle. Conflicting prior studies proposed mitochondrial complex I or various cytosolic targets for metformin action, but we show that the compound limits respiration and citric acid cycle activity in isolated mitochondria, indicating that at least for these effects, the mitochondrion is the

Induction of mitochondrial permeability transition (MPT) and cytosolic translocation of cytochrome C are considered essential components of the apoptotic pathway. Hence, there is the realization that mitochondrial- specific drugs could have potential for use as chemotherapeutic agents to trigger apoptosis In tumor cells. Recently, we showed that photoproducts of merocyanine 540 (pMC540) induced tumor cell apoptosis. In this study, we focused on identifying mitochondrial-specific compounds from pMC540 and studied their apoptotic potential. One purified fraction, C5, induced a drop In mitochondrial transmembrane potential and cytosolic translocation of cytochrome C in HL60 human leukemia cells. Moreover, the addition of C5 to purified rat liver mitochondria induced MPT as indicated by mitochondrial matrix swelling, which was completely inhibited by cyclosporin A, an inhibitor of the inner-membrane pore. Supernatant of C5-treated mitochondria showed a dose-dependent increase in cytochrome C, which ...

Electron Transport Chain and Energy Production In cellular biology, the electron transport chain is one of the steps in your cells processes that make energy from the foods you eat.à It is the third step of aerobic cellular respiration. Cellular respiration is the term for how your bodys cells make energy from food consumed. The electron transport chain is where most of the energy cells need to operate is generated. This chain is actually a series of protein complexes and electron carrier molecules within the inner membrane of cell mitochondria, also known as the cells powerhouse. Oxygen is required forà aerobic respirationà as the chain terminates with the donation of electrons to oxygen.à Key Takeaways: Electron Transport Chain The electron transport chain is a series of protein complexes and electron carrier molecules within the inner membrane of mitochondria that generate ATP for energy.Electrons are passed along the chain from protein complex to protein complex until they are donated to ...

Small W.C., McAlister-Henn L.. The reoxidation of NADH generated in reactions within the mitochondrial matrix of Saccharomyces cerevisiae is catalyzed by an NADH dehydrogenase designated Ndi1p (C. A. M. Marres, S. de Vries, and L. A. Grivell, Eur. J. Biochem. 195:857-862, 1991). Gene disruption analysis was used to examine possible metabolic functions of two proteins encoded by open reading frames having significant primary sequence similarity to Ndi1p. Disruption of the gene designated NDH1 results in a threefold reduction in total mitochondrial NADH dehydrogenase activity in cells cultivated with glucose and in a fourfold reduction in the respiration of isolated mitochondria with NADH as the substrate. Thus, Ndh1p appears to be a mitochondrial dehydrogenase capable of using exogenous NADH. Disruption of a closely related gene designated NDH2 has no effect on these properties. Growth phenotype analyses suggest that the external NADH dehydrogenase activity of Ndh1p is important for optimum ...

TY - JOUR. T1 - Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors. AU - Luo, Xu. AU - Budihardjo, Imawati. AU - Zou, Hua. AU - Slaughter, Clive. AU - Wang, Xiaodong. PY - 1998/8/21. Y1 - 1998/8/21. N2 - We report here the purification of a cytosolic protein that induces cytochrome c release from mitochondria in response to caspase-8, the apical caspase activated by cell surface death receptors such as Fas and TNF. Peptide mass fingerprinting identified this protein as Bid, a BH3 domain- containing protein known to interact with both Bcl2 and Bax. Caspase-8 cleaves Bid, and the COOH-terminal part translocates to mitochondria where it triggers cytochrome c release. Immunodepletion of Bid from cell extracts eliminated the cytochrome c releasing activity. The cytochrome c releasing activity of Bid was antagonized by Bcl2. A mutation at the BH3 domain diminished its cytochrome c releasing activity. Bid, ...

Complex I and complex III are the major sites of ROS generation in mitochondria15; however, the site responsible for volatile anesthetic-induced ROS generation remains undefined. The following evidence supports the contention that complex I is a source of isoflurane-induced ROS: isoflurane increases ROS generation with complex I- but not complex II-linked substrates in SMPs (fig. 5); and isoflurane only alters activity of complex I, but not of the other complexes in solubilized mitochondria. However, isoflurane-induced ROS generation in isolated mitochondria was not detected in our experiments when complex I-linked substrates were used. This apparent discrepancy observed in isolated mitochondria compared with submitochondrial particles may have occurred because ROS generated at complex I site are released into the mitochondrial matrix where they rapidly react with manganese superoxide dismutase before interacting with detection reagent in the buffer.15Interestingly, in the presence of rotenone, ...

Title:Direct Quantification of Mitochondria and Mitochondrial DNA Dynamics. VOLUME: 13 ISSUE: 14. Author(s):Yasutomo Nomura. Affiliation:Department of Systems Life Engineering, Maebashi Institute of Technology, 460-1 Kamisadori, Maebashi, Japan.. Keywords:Mitochondria, mtDNA, image correlation spectroscopy, fusion, fission, cytoskeleton, fluorescence microscopy, major organelles, cell, cytoskeletal tracks , mitochondrial DNA dynamics, metabolic diseases, compounds, heterogeneous environment. Abstract:Mitochondria are known to be one of major organelles within a cell and to play a crucial role in many cellular functions. These organelles show the dynamic behaviors such as fusion, fission and the movement along cytoskeletal tracks. Besides mitochondria, mitochondrial DNA is also highly motile. Molecular analysis revealed that several proteins are involved in mitochondria and mitochondrial DNA dynamics. In addition to the degeneration of specific nerves with high energy requirement, mutation of ...

We show that the ISE1 gene encodes a mitochondria-localized DEAD-box RNA helicase. Absence of functional ISE1 leads to increased intercellular transport of large dextrans during Arabidopsis embryogenesis. In support of the role of ISE1 in PD-mediated intercellular transport, PD are altered in ise1 mutant embryos; specifically, ise1 mutants have more branched and twinned PD than wild-type embryos, suggesting that PD biogenesis may be up-regulated in ise1-1 mutants. Further, the ise1 phenotype can be recapitulated in mature leaf tissues by silencing the ISE1 gene; ISE1-silenced tissues exhibit increased intercellular movement of TMV P30-2XGFP. Thus, the pathway or process disrupted by the loss of ISE1 function affects transport via PD in mature and embryonic tissues. We show that ISE1 is localized to mitochondria and that the N terminus of ISE1 contains a mitochondria-targeting sequence. The disruption of mitochondrial function in ise1 mutants is supported by the failure of their mitochondria to ...

The polyamine spermine is transported into the matrix of various types of mitochondria by a specific uniporter system identified as a protein channel. This mechanism is regulated by the membrane potential; other regulatory effectors are unknown. This study analyzes the transport of spermine in the presence of peroxides in both isolated rat liver and brain mitochondria, in order to evaluate the involvement of the redox state in this mechanism, and to compare its effect in both types of mitochondria. In liver mitochondria peroxides are able to inhibit spermine transport. This effect is indicative of redox regulation by the transporter, probably due to the presence of critical thiol groups along the transport pathway, or in close association with it, with different accessibility for the peroxides and performing different functions. In brain mitochondria, peroxides have several effects, supporting the hypothesis of a different regulation of spermine transport. The fact that peroxovanadate can inhibit

In cell biology, a mitochondrion is a membrane-enclosed organelle found in most eukaryotic cells. Mitochondria are often described as cellular power plants because they generate most of the cells supply of adenosine triphosphate (ATP), used as a source of the chemical energy. In addition to supplying cellular energy, mitochondria are involved in a range of other processes, such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth. This book reviews research on the mitochondrial metabolism in age-related neurodegenerative disorders such as Alzheimers and Parkinsons disease; mitochondria and aging; apoptosis and peritoneal injury; diabetes, mitochondria and brain endothelium dysfunction as a dangerous triad for neurodegeneration ...

The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. Here, we have demonstrated a striking morphological change of mitochondria in experimental models of renal ischemia/reperfusion and cisplatin-induced nephrotoxicity. This change contributed to mitochondrial outer membrane permeabilization, release of apoptogenic factors, and consequent apoptosis. Following either ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was observed prior to cytochrome c release and apoptosis. This mitochondrial fragmentation was inhibited by Bcl2 but not by caspase inhibitors. Dynamin-related protein 1 (Drp1), a critical mitochondrial fission protein, translocated to mitochondria early during tubular cell injury, and both siRNA knockdown of Drp1 and expression of a dominant-negative Drp1 attenuated mitochondrial fragmentation, cytochrome c release, caspase activation, and apoptosis. Further ...

TY - JOUR. T1 - Direct evidence for coherent low velocity axonal transport of mitochondria. AU - Miller, Kyle E.. AU - Sheetz, Michael. PY - 2006/5/8. Y1 - 2006/5/8. N2 - Axonal growth depends on axonal transport. We report the first global analysis of mitochondrial transport during axonal growth and pauses. In the proximal axon, we found that docked mitochondria attached to the cytoskeletal framework that were stationary relative to the substrate and fast axonal transport fully accounted for mitochondrial transport. In the distal axon, we found both fast mitochondrial transport and a coherent slow transport of the mitochondria docked to the axonal framework (low velocity transport [LVT]). LVT was distinct from previously described transport processes; it was coupled with stretching of the axonal framework and, surprisingly, was independent of growth cone advance. Fast mitochondrial transport decreased and LVT increased in a proximodistal gradient along the axon, but together they generated a ...

Flight Muscle Mitochondria This image is of non-human tissue. Flight muscle is the most powerful type of muscle, to cope with the aerobic demands of flying the balance of muscle fibres and mitochondria has to be optimal. Here we see flight muscle from a bird in a transverse cut. Mitochondria generate the energy that cells need to function. The energy made by the mitochondria is in the form of a chemical called adenosine triphosphate or ATP. The mitochondria are the pink/red structures in this image. Cellular level art, paint on silk, digitised.

Mitofilin, also known as heart muscle protein, is a recently identified mitochondrial protein. We have isolated two human cDNAs that encode different isoforms of mitofilin. Using reverse PCR, we provide evidence that both isoforms are derived by alternative splicing and encode two proteins of 88 and 90 kDa that are detected in immunoblot analyses with mitofilin-specific antibodies, Immunofluorescence microscopy, fractionating of human osteosarcoma cells, and protease protection experiments with isolated mitochondria and mitoplasts indicate that mitofilin is an integral membrane protein of the inner mitochondrial membrane. S-35-labeled mitofilin is transported into isolated yeast mitochondria in a reaction that depends on the membrane potential across the inner mitochondrial membrane (Delta Psi). During mitochondrial in vitro import, mitofilin is proteolytically processed to the mature protein that is also detected in cellular fractions, indicating that the amino-terminal leader sequence is ...

VARECHA, Miroslav et al. Knockdown of apoptosis-inducing factor disrupts function of respiratory complex I. Biocell [online]. 2012, vol.36, n.3, pp.121-126. ISSN 0327-9545.. Recent findings suggest that apoptotic protein apoptosis-inducing factor (AIF) may also play an important non-apoptotic function inside mitochondria. AIF was proposed to be an important component of respiratory chain complex I that is the major producer of superoxide radical. The possible role of AIF is still controversial. Superoxide production could be used as a valuable measure of complex I function, because the majority of superoxide is produced there. Therefore, we employed superoxide-specific mitochondrial fluorescence dye for detection of superoxide production. We studied an impact of AIF knockdown on function of mitochondrial complex I by analyzing superoxide production in selected cell lines. Our results show that tumoral telomerase-positive (TP) AIF knockdown cell lines display significant increase in superoxide ...

Wld(S) (slow Wallerian degeneration) is a remarkable protein that can suppress Wallerian degeneration of axons and synapses, but how it exerts this effect remains unclear. Here, using Drosophila and mouse models, we identify mitochondria as a key site of action for Wld(S) neuroprotective function. Targeting the NAD(+) biosynthetic enzyme Nmnat to mitochondria was sufficient to fully phenocopy Wld(S), and Wld(S) was specifically localized to mitochondria in synaptic preparations from mouse brain. Axotomy of live wild-type axons induced a dramatic spike in axoplasmic Ca(2+) and termination of mitochondrial movement-Wld(S) potently suppressed both of these events. Surprisingly, Wld(S) also promoted increased basal mitochondrial motility in axons before injury, and genetically suppressing mitochondrial motility in vivo dramatically reduced the protective effect of Wld(S). Intriguingly, purified mitochondria from Wld(S) mice exhibited enhanced Ca(2+) buffering capacity. We propose that the enhanced ...

Curated}} {{Biorealm Genus}} [[Image:mitochondria.gif,thumb,400px,right,Mitochondria. Courtesy of [http://employees.csbsju.edu/hjakubowski/classes/ch331public/ch331.html Dr. Henry Jakubowski.]]] ==Classification== ===Higher order taxa:=== Bacteria; Proteobacteria; Alphaproteobacteria; Rickettsiales; Rickettsiaceae; Rickettsieae ===Species:=== Most species of eukaryotes, including plant, fungi, and animal cells contain mitochondria. Mitochondria are phylogenically most closely related to the microbe Rickettsia prowazekii. They are thought to be monophyletic. {, , height=10 bgcolor=#FFDF95 align=center , NCBI: [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=780&lvl=3&lin=f&keep=1&srchmode=1&unlock Taxonomy] Genome (examples): -,font size=2>[http://www.ncbi.nlm.nih.gov/genomes/framik.cgi?db=genome&gi=17601 Drosophila simulans ],/font>,font size=2>[http://www.ncbi.nlm.nih.gov/genomes/framik.cgi?db=genome&gi=17601 mitochondria],/font> -,font ...

Arsenic exposure mainly through food and water has been shown to be associated with increased incidence of numerous cancers and non-cancer harmful health. It is also used in cancer chemotherapy and treatment of several cancer types due to its apoptogenic effects in the various cancer and normal cell lines. We have already reported that liver is the storage site and important target organ in As (III) toxicity and recently, it has been suggested that hepatic toxicity of arsenic could be resulted from impairment of the liver mitochondria. In this study, interaction of As (III) with freshly isolated rat mitochondria was investigated. We determined different mitochondrial toxicity factors as well as mitochondrial sources of ROS formation using specific substrates and inhibitors following addition of As (III) to the mitochondria. Our results showed that arsenic (III) increased mitochondrial ROS formation, lipid peroxidation and mitochondrial membrane potential collapse, cytochrome c release and mitochondrial

Mitochondrial autophagy is an important adaptive stress response and can be modulated by various key molecules. A previous study found that the regulator of calcineurin 1-1L (Rcan1-1L) may regulate mitochondrial autophagy and cause mitochondria degradation in neurocytes. However, the effect of Rcan1-1L on cardiomyocytes has not been determined. In the present study, we aimed to investigate the role of Rcan1-1L in angiotensin II (Ang II)-exposed human cardiomyocytes. Above all, Human adult cardiac myocytes (HACMs) were exposed to 200 nmol/L Ang II for 4 days. Enhanced H{sub 2}O{sub 2} production, cytochrome C release and mitochondrial permeability were observed in these cells, which were blocked by valsartan. Consistently, Ang II exposure significantly reduced cardiomyocyte viability. However, transfection of Rcan1-1L vector promoted cell viability and ameliorated the apoptosis caused by Ang II. Rcan1-1L clearly promoted mitochondrial autophagy in HACMs, with elevated autophagy protein (ATG) 5 ...

Oxidative phosphorylation was measured polarographically in mitochondria isolated from normal ventricles and from the ventricles of guinea pigs and cats with experimental heart failure produced by constriction of the aorta or pulmonary artery. The presence of heart failure was proved by the study of myocardial mechanics in vitro, by cardiac catheterization, and by postmortem examination. Mitochondria from failing ventricles had normal oxidative phosphorylation, and P-O ratios, respiratory control, oxygen consumption and ATPase activity did not differ from those of mitochondria from normal hearts. Results were the same whether incubations were performed at 25° or 37°C and whether glutamate or pyruvate and malate were used as the substrate. Mitochondria showed functional deterioration, probably due to fatty acid accumulation, when incubated for more than 10 min at 37°C or when isolated from hearts made hypoxic in vivo for as little as 3 min. The results of this study suggest that decreased ...

Image: (A) Healthy Cells with normal mitochondria. (B) BTHS cells with elongated and abnormal mitochondria. Image copyright by International Journal of Molecular Sciences, PMID 31336787. Promising results were recently published demonstrating gene replacement can lead to improved mitochondrial structure and function, signaling the possibility to reverse the underlying biology of Barth syndrome. Using cells obtained from individuals with different TAZ mutations of varied severity in Barth syndrome, Suzuki-Hatano et al. tested the impact of AAV-TAZ transduction in a cellular model and found that providing a functional copy of tafazzin improves mitochondrial processes in cells affected by Barth syndrome.. Alongside previously studies analyzing human proteins and the impact of AAV-TAZ transduction in a Barth syndrome (knockdown) mouse model, the collaborative research team at the University of Florida and Washington University continue to generate a body of work that will support an investigational ...

Mitochondria are fascinating organelles regulating many critical cellular processes for skeletal muscle physiology. Indeed, they play central roles in muscle cell metabolism, energy supply, the regulation of energy-sensitive signaling pathways, reactive oxygen species (ROS) production/signaling, calcium homeostasis and the regulation of apoptosis [1]. Given these multifaceted roles of mitochondria in fundamental aspects of skeletal muscle cell physiology, it is not surprising that mitochondrial dysfunction has been implicated in a large number of adverse conditions affecting skeletal muscle health. This includes for instance the aging-related loss of muscle mass and function [2-9], disuse-induced muscle atrophy [10], ventilator-induced diaphragmatic dysfunction [11], Duchenne and collagen muscular dystrophies [12, 13], long-term muscle dysfunction induced by chemotherapy treatment [14, 15], and the development of insulin resistance [16]. While the importance of normal mitochondrial function is well

TY - JOUR. T1 - Dissociation of Cytochrome c from the Inner Mitochondrial Membrane during Cardiac Ischemia. AU - Czerski, Lech W.. AU - Szweda, Pamela A.. AU - Szweda, Luke I.. PY - 2003/9/5. Y1 - 2003/9/5. N2 - Mitochondria isolated from ischemic cardiac tissue exhibit diminished rates of respiration and ATP synthesis. The present study was undertaken to determine whether cytochrome c release was responsible for ischemia-induced loss in mitochondrial function. Rat hearts were perfused in Langendorff fashion for 60 min (control) or for 30 min followed by 30 min of no flow ischemia. Mitochondria isolated from ischemic hearts in a buffer containing KCl exhibited depressed rates of maximum respiration and a lower cytochrome c content relative to control mitochondria. The addition of cytochrome c restored maximum rates of respiration, indicating that the release of cytochrome c is responsible for observed declines in function. However, mitochondria isolated in a mannitol/sucrose buffer exhibited no ...

TY - JOUR. T1 - Activation of mitogen-activated protein kinases by lysophosphatidylcholine- induced mitochondrial reactive oxygen species generation in endothelial cells. AU - Watanabe, Nobuo. AU - Zmijewski, Jaroslaw W.. AU - Takabe, Wakako. AU - Umezu-Goto, Makiko. AU - Le Goffe, Claire. AU - Sekine, Azusa. AU - Landar, Aimee. AU - Watanabe, Akira. AU - Aoki, Junken. AU - Arai, Hiroyuki. AU - Kodama, Tatsuhiko. AU - Murphy, Michael P.. AU - Kalyanaraman, Raman. AU - Darley-Usmar, Victor M.. AU - Noguchi, Noriko. PY - 2006/5. Y1 - 2006/5. N2 - Lysophosphatidylcholine (lysoPC) evokes diverse biological responses in vascular cells including Ca2+ mobilization, production of reactive oxygen species, and activation of the mitogen-activated protein kinases, but the mechanisms linking these events remain unclear. Here, we provide evidence that the response of mitochondria to the lysoPC-dependent increase in cytosolic Ca2+ leads to activation of the extracellular signal-regulated kinase (ERK) ...

PINK1 and Parkin are established mediators of mitophagy, the selective removal of damaged mitochondria by autophagy. PINK1 and Parkin have been proposed to act as tumor suppressors, as loss-of-function mutations are correlated with enhanced tumorigenesis. However, it is unclear how PINK1 and Parkin act in coordination during mitophagy to influence the cell cycle. Here we show that PINK1 and Parkin genetically interact with proteins involved in cell cycle regulation, and loss of PINK1 and Parkin accelerates cell growth. PINK1- and Parkin-mediated activation of TBK1 at the mitochondria during mitophagy leads to a block in mitosis due to the sequestration of TBK1 from its physiological role at centrosomes during mitosis. Our study supports a diverse role for the far-reaching, regulatory effects of mitochondrial quality control in cellular homeostasis and demonstrates that the PINK1/Parkin pathway genetically interacts with the cell cycle, providing a framework for understanding the molecular basis ...

Mitochondria are essential for cellular function, providing ATP for energy and regulating a number of key metabolic processes including apoptosis and calcium homeostasis. The consumption of oxygen by the mitochondrial electron transport chain leads to production of ATP but also to release of electrons that can lead to the generation of free radical species and oxidative damage. Thus, proper function and control of mitochondrial is critical. Mitochondrial function has long been thought to be compromised during aging leading to alter physiologic function and age related pathologies. Our work on sarcopenia described above suggests that altered mitochondrial function and increased generation of reactive oxygen species can contribute to the physiologic decline seen in sarcopenia and ALS. However, in other studies we have shown that altered mitochondrial function can have beneficial effects on metabolism. For example, mice lacking Surf1, a mitochondrial electron transport chain protein assembly ...

Mouse Anti-Bovine Complex V (F1F0 ATP Synthase) Heart Mitochondria Monoclonal Antibody, Unconjugated, Clone 12F4AD8AF8 from MitoScience LLC,100 g monoclonal antibody which can immunocapture up to 50 g of Complex V from heart mitochondria. Also included are 2 mg of bovine heart mitochondria for control immunocapture. The Complex V immunocapture kit allows isolation of the ATP synthase complex (E.C. 3.6.3.14) from small amounts of tissue,biological,biology supply,biology supplies,biology product

Identification of the SLIK complex.We have presented evidence that in yeast two highly related HAT complexes exist, SAGA and SLIK. Consistent with this observation, other studies have previously pointed to the putative existence of two distinct high-molecular-weight Ada-containing complexes (22, 25, 50). A combination of mass spectrometry and Western blotting of highly purified SLIK complex identified a similar set of Ada, Spt, TAFII, and Tra1 proteins as components, which were previously identified in SAGA. Both SAGA and SLIK are high-molecular-weight multiprotein complexes with very similar substrate specificities, preferentially modifying the same lysine residues in the nucleosomal histone H3 tail. However, Spt8 and Rtg2 were identified as unique components of SAGA and SLIK, respectively, suggesting that each complex has a distinct function that is not related to histone substrate specificity.. The RTG1, RTG2, and RTG3 genes are central players in the retrograde response pathway (26, 35). ...

Background: Although the bio kinetics, metabolism and chemical toxicity of Atorvastatin are well known, until recently little attention was paid to the potential neurotoxic effect of Atorvastatin (Atv). Regarding the concrete evidences indicating Atv may reduce Coenzyme Q10 (CoQ10) levels through blockage of metalonate cycle, the present work aims to determine if Atorvastatin may provide toxic effects on brain mitochondria and whether its supplementation with two lipidicantioxidants, CoQ10 and Vit E may improve such outcomes. Methods: to evaluate mitochondrial toxicity, male NMRI mice were first treated with Atorvastatin(bo; 20 and 60 mg/kg) every other day with or without supplementation with CoQ10 (200 mg/kg) or Vit E (40 u/kg). After a period of 4 weeks, the animals were euthanized and brain cortices were harvested ad subjected to mitochondria isolation procedure. ROS release, mitochondrial membrane potential (MMP) and cytochrome c release were performed to precisely address the probable

Dedkova EN, Ji X, Lipsius SL, Blatter LA. Mitochondrial calcium uptake stimulates nitric oxide production in mitochondria of bovine vascular endothelial cells. Am J Physiol Cell Physiol. 2004 Feb; 286(2):C406-15 ...

RNA import into mammalian mitochondria is considered essential for replication, transcription, and translation of the mitochondrial genome but the pathway(s) and factors that control this import are poorly understood. Previously, we localized polynucleotide phosphorylase (PNPASE), a 3 --, 5 exoribonuclease and poly-A polymerase, in the mitochondrial intermembrane space, a location lacking resident RNAs. Here, we show a new role for PNPASE in regulating the import of nuclear-encoded RNAs into the mitochondrial matrix. PNPASE reduction impaired mitochondrial RNA processing and polycistronic transcripts accumulated. Augmented import of RNase P, 5S rRNA, and MRP RNAs depended on PNPASE expression and PNPASE-imported RNA interactions were identified. PNPASE RNA processing and import activities were separable and a mitochondrial RNA targeting signal was isolated that enabled RNA import in a PNPASE-dependent manner. Combined, these data strongly support an unanticipated role for PNPASE in mediating ...

Senescence is a major factor to increase oxidant stress in mitochondria, which contributes to the pathogenesis of heart diseases. We postulated that scavenging effect of superoxide targeted in mitochondria would have benefit in the aged heart. Increased levels of superoxide and NADPH oxidase activity were appeared in cardiac myocytes isolated from old mice (70 W) compared to those in young mice (8 W) (superoxide: 2.6±0.4 vs. 1.2±0.2 nmol/mg protein; NADPH oxidase activity: 2654±282 vs. 1124±156 RLU, p,0.01, n=16, respectively). In old mice treated with mitochondria-targeted antioxidant, MitoTEMPO, co-infusion using minipump (180 μg/kg/day, 28 days), levels of superoxide and NADPH oxidase activity decreased (0.2±0.2 nmol/mg protein and 342±45 RLU, p,0.01, respectively). Treatment with MitoTEMPO improved left ventricular ejection fraction from 48±5% to 62±5% (p,0.01) with old mice in echocardiography. Endothelium-dependent coronary artery vasodilation, eNOS and Sirt1 levels were lower in ...

The effect of cAMP on Ca²⁺ release was reinvestigated in the present study based on the findings of Lehninger et al (1978) and Christiansen (1977). Cyclic AMP caused Ca²⁺ release provided that palmitoyl CoA or palmitoylcarnitine were substrates and that the mitochondria prepared from fed rats were used within 1 hr after isolation. It was also noted in this study that the mitochondria isolated from starved rats had a lower NADH/NAD⁺ ratio and released their Ca²⁺ earlier than the mitochondria from fed rats. It was suggested that cAMP stimulates Ca²⁺ release from the mitochondria presumably by altering the redox state of the mitochondrial pyridine nucleotides.. ...

The structure, distribution and possible roles of mitochondria in growing pollen tubes is reviewed. Diverse microscopical methods have been applied to the analysis of mitochondria in pollen, with a predominance in recent years on vital fluorescent probes. We review the application of different dyes to pollen tubes, with a special emphasis on the ratiometric dye JC-1. Morphometric data shows a concentration of mitochondria in the subapical area of pollen tubes, apparently with more frequency of mitochondria with membrane depolarization when compared with the rest of the tube. Remarkably, data from various species and from transcriptomics indicates that different species may have different respiratory adaptations, ranging from high oxygen consumption in the early steps of germination, to energy production and growth on almost anoxic conditions. Various studies also showed that the pollen of many species is refractory to some common respiration inhibitors, including the ones from the alternative ...

TY - JOUR. T1 - Mitochondrial dysfunction in aging and Alzheimers disease. T2 - Strategies to protect neurons. AU - Reddy, P (Hemachandra). PY - 2007/10. Y1 - 2007/10. N2 - Recent structural and functional studies of mitochondria have revealed that abnormalities in mitochondria may lead to mitochondrial dysfunction in aged individuals and those with neurodegenerative diseases, including Alzheimers disease (AD). Molecular, cellular, and biochemical studies of animal models of aging and AD have provided compelling evidence that mitochondria are involved in AD development and progression. Further, a role for mitochondrial dysfunction in AD is supported by studies of neurons from autopsy specimens of patients with AD, transgenic AD mice, and neuronal cells expressing human AD mutation, which have revealed that amyloid beta (Aβ) enters mitochondria early in the disease process and disrupts the electron-transport chain, generates reactive oxygen species, and inhibits the production of cellular ATP, ...

Mitochondrial dysfunction contributes to cardiac ischemia-reperfusion (IR) injury but volatile anesthetics (VA) may alter mitochondrial function to trigger cardioprotection. We hypothesized that the VA isoflurane (ISO) mediates cardioprotection in part by altering the function of several respiratory and transport proteins involved in oxidative phosphorylation (OxPhos). To test this we used fluorescence spectrophotometry to measure the effects of ISO (0, 0.5, 1, 2 mM) on the time-course of interlinked mitochondrial bioenergetic variables during states 2, 3 and 4 respiration in the presence of either complex I substrate K+-pyruvate/malate (PM) or complex II substrate K+-succinate (SUC) at physiological levels of extra-matrix free Ca2 + (~ 200 nM) and Na+ (10 mM). To mimic ISO effects on mitochondrial functions and to clearly delineate the possible ISO targets, the observed actions of ISO were interpreted by comparing effects of ISO to those elicited by low concentrations of inhibitors that act at each

Maternal smoking has been recognized as a common cause of low birth weight, preterm birth and the decrease of gestational age period. Unfortunately, there is an increasing interest within public especially woman in Iran in the tobacco products consumption. On the other hand, the deleterious effect of maternal smoking on human fetus in pregnancy period especially in the first trimester encouraged us to investigate toxicity mechanisms of cigarette smoke on mouse fetus mitochondria. For this purpose different concentrations of standardized cigarette smoke extract (1, 10 and 100%) were administrated on mitochondria isolated from fetus of NMRI mice on the 15 day of gestation. Our results showed a significant increase in ROS formation, lipid peroxidation, mitochondrial membrane potential collapse, mitochondrial swelling and finally a decrease in ATP concentration in the CSE-treated isolated fetus mitochondria. Our results suggest that CSE-induced embryo toxicity is the result of disruptive effect on

Limb remote ischemic preconditioning (RIPC) is an effective means of protection against ischemia/reperfusion (IR)-induced injury to multiple organs. Many studies are focused on identifying endocrine mechanisms that underlie the cross-talk between muscle and RIPC-mediated organ protection. We report that RIPC releases irisin, a myokine derived from the extracellular portion of fibronectin domain-containing 5 protein (FNDC5) in skeletal muscle, to protect against injury to the lung. Human patients with neonatal respiratory distress syndrome show reduced concentrations of irisin in the serum and increased irisin concentrations in the bronchoalveolar lavage fluid, suggesting transfer of irisin from circulation to the lung under physiologic stress. In mice, application of brief periods of ischemia preconditioning stimulates release of irisin into circulation and transfer of irisin to the lung subjected to IR injury. Irisin, via lipid raft-mediated endocytosis, enters alveolar cells and targets ...

The initiating events that lead to the induction of apoptosis mediated by the chemopreventative agent β-phenyethyl isothiocyanate (PEITC) have yet to be elucidated. In the present investigation, we examined the effects of PEITC on mitochondrial function and apoptotic signaling in hepatoma HepG2 cells and isolated rat hepatocyte mitochondria. PEITC induced a conformational change in Bax leading to its translocation to mitochondria in HepG2 cells. Bax accumulation was associated with a rapid loss of mitochondrial membrane potential (Δψm), impaired respiratory chain enzymatic activity, release of mitochondrial cytochrome c and the activation of caspase-dependent cell death. Caspase inhibition did not prevent Bax translocation, the release of cytochrome c or the loss of Δψ m, but blocked caspase-mediated DNA fragmentation and cell death. To determine whether PEITC dependent Bax translocation caused loss of Δψm by the activation of the mitochondrial permeability transition (MPT), we examined ...