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A list of all pages that have property "Has abstract" with value "13th ÖGMBT Annual Meeting, Virtual, 2021". Since there have been only a few results, also nearby values are displayed.

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  • Paeaebo 2014 Basic Books  + ('The Neanderthals live on in many of us to'The Neanderthals live on in many of us today' (p 199).</br></br>Neanderthal Man tells the story of geneticist Svante Pääbo's mission to answer this question, and recounts his ultimately successful efforts to genetically define what makes us different from our Neanderthal cousins. Beginning with the study of DNA in Egyptian mummies in the early 1980s and culminating in the sequencing of the Neanderthal genome in 2010, Neanderthal Man describes the events, intrigues, failures, and triumphs of these scientifically rich years through the lens of the pioneer and inventor of the field of ancient DNA.</br></br>We learn that Neanderthal genes offer a unique window into the lives of our hominin relatives and may hold the key to unlocking the mystery of why humans survived while Neanderthals went extinct. Drawing on genetic and fossil clues, Pääbo explores what is known about the origin of modern humans and their relationship to the Neanderthals and describes the fierce debate surrounding the nature of the two species' interactions. His findings have not only redrawn our family tree, but recast the fundamentals of human history—the biological beginnings of fully modern ''Homo sapiens'', the direct ancestors of all people alive today.</br></br>A riveting story about a visionary researcher and the nature of scientific inquiry, Neanderthal Man offers rich insight into the fundamental question of who we are.to the fundamental question of who we are.)
  • Sipos 2005 Cell Mol Neurobiol  + ((1) Endothelial cells are permanently chal(1) Endothelial cells are permanently challenged by altering pH in the blood, and oxidative damage could also influence the intracellular pH (pH(i)) of the endothelium. Cerebral microvascular endothelial cells form the blood-brain barrier (BBB) and pH(i) regulation of brain capillary endothelial cells is important for the maintenance of BBB integrity. The aim of this study was to address the pH regulatory mechanisms and the effect of an acute exposure to hydrogen peroxide (H2O2) on the pH regulation in primary rat brain capillary endothelial (RBCE) cells The RBCE monolayers were loaded with the fluorescent pH indicator BCECF and pH(i) was monitored by detecting the fluorescent changes. (2) The steady-state pH(i) of RBCE cells in HEPES-buffer (6.83 +/- 0.1) did not differ significantly from that found in bicarbonate-buffered medium (6.90 +/- 0.08). Cells were exposed to NH4CI to induce intracellular acidification and then the recovery to resting pH was studied. Half-recovery time after NH4Cl prepulse-induced acid load was significantly less in the bicarbonate-buffered medium than in the HEPES-medium, suggesting that in addition to the Na+ / H+ exchanger, HCO3- / Cl- exchange mechanism is also involved in the restoration of pH(i) after an intracellular acid load in primary RBCE cells. We used RT-PCR-reactions to detect the isoforms of Na+ / H+ exchanger gene family (NHE). NHE-1 -2, -3 and -4 were equally present, and there was no significant difference in the relative abundance of the four transcripts in these cells. (3) No pH(i) recovery was detected when the washout after an intracellular acid load occurred in nominally Na+ -free HEPES-buffered medium or in the presence of 10 microM 5-(N-ethyl-N-isopropyl)amiloride (EIPA), a specific inhibitor of Na+ / H+ exchanger. The new steady-state pH(i) were 6.37 +/- 0.02 and 6.60 +/- 0.02, respectively. (4) No detectable change was observed in the steady-state pH(i) in the presence of 100 microM H2O2; however, recovery from NH4Cl prepulse-induced intracellular acid load was inhibited when H2O2 was present in 50 or 100 microM concentration in the HEPES-buffered medium during NH4Cl washout. These data suggest that H2O2 is without effect on the activity of Na+ / H+ exchanger at rest, but could inhibit the function of the exchanger after an intracellular acid load.xchanger after an intracellular acid load.)
  • MiPNet25.14 TPP Analysis Template  + ((2020) Excel template for TPP data analys(2020) Excel template for TPP data analysis. Mitochondr Physiol Network 25.14(01):1-8. </br><br/></br></br><div style="padding:0px;border: 1px solid #aaaaaa;margin-bottom:0px;margin-right:10px"></br><div style="font-size:100%;font-weight:bold;padding:0.2em;padding-right: 0.4em;padding-left: 0.4em;background-color:#eeeeee;border-bottom:1px solid #aaaaaa;text-align:left;"></br>[[Image:O2k-support system.jpg|right|150px|link=http://wiki.oroboros.at/index.php/O2k-technical_support_and_open_innovation|O2k-technical support and open innovation]]</br>: <big>Open the '''pdf document''' above.</big></br></div></br><div style="background-color:#ffffff;padding-top:0.2em;padding-right: 0.4em;padding-bottom: 0.2em;padding-left: 0.4em;"></br>::::» Current O2k-series: '''[https://www.oroboros.at/index.php/product-category/products/o2k-packages/ NextGen-O2k Series XB and O2k Series J]'''</br>::::» Current software versions DatLab 8.0: [[MitoPedia: DatLab]]</br>::::* ''Further details:'' '''» [[MitoPedia: O2k-Open Support]]'''</br></div></br></div></br>:» Product: [[DatLab]], [[Oroboros O2k]], [[Oroboros O2k-Catalogue |O2k-Catalogue]]oboros O2k-Catalogue |O2k-Catalogue]])
  • Kagawa 1971 J Biol Chem  + ( * Amorphous membrane fragments depleted i</br>* Amorphous membrane fragments depleted in P-lipids and cytochrome oxidase were isolated from bovine heart mitochondria and were reconstituted with P-lipids and coupling factors to yield vesicular structures. These vesicles catalyzed a 32Pi—ATP exchange and showed an induced enhancement of anilinonaphthalene sulfonate fluorescence on addition of ATP</br></br>* 32Pi—ATP exchange and fluorescence enhancement were abolished by uncouplers of oxidative phosphorylation and by energy transfer inhibitors. The ATPase activity was inhibited by energy transfer inhibitors, but stimulated by uncouplers or by the combined action of nigericin and valinomycin in the presence of K+. Both ATPase activity and 32Pi—ATP exchange were inhibited by a specific antibody against coupling factor 1.</br></br>* It was shown that the reconstitution of vesicular structures with functional activity required several hours. Rapid reconstitution resulted in inactive vesicles. Evidence for the formation of new vesicles from solubilized P-lipids was obtained by demonstrating inclusion of macromolecules such as 14C-labeled inulin or ferritin which could not be removed by washing.</br>itin which could not be removed by washing. )
  • Cannon 2015 Fatty Acid Oxidation O2k-Network Discussion Forum  + ( *Saponin permeabilized skeletal muscle fi</br>*Saponin permeabilized skeletal muscle fiber bundles</br></br>*'''Protocol''':</br>#0.5mM Malate</br>#50 µM palmitoyl-CoA + 2mM carnitine</br>#5mM ADP</br>#From here on out, various combinations for titration protocol</br></br>*Coupling states:</br>#LEAK_M+Palmitoylcarnitine</br>#P_M+Palmitoylcarnitine</br>#P_M+Palmitoylcarnitine+S</br>#E_O+CCCP titrations</br>#E_S+Rot</br>#ROX_AntimycinA</br>_O+CCCP titrations #E_S+Rot #ROX_AntimycinA )
  • Nernst 1921 Nobel Lecture  + (.. From the start of my scientific career .. From the start of my scientific career the galvanic cell, the first form of which, the Volta pile, popularized physics in a single stroke and at the same time presented us with so many problems, appeared to me to merit especially further study. ..</br></br>It was particularly disillusioning to find a man like Helmholtz returning repeatedly throughout his scientific career to his first love, the galvanic cell, which he had courted in his great youthful work "Erhaltung der Kraft" (The conservation of energy), without however succeeding in finding a satisfactory solution.</br></br>As often in natural science the picture changed quite suddenly. New fruitful concepts appeared, through the interplay and extension of which most of the darkness has been to a large extent dispelled in a single stroke. Such means were Van ’t Hoff’s theory of osmotic pressure, Arrhenius’ theory of electrolytic dissociation, and finally many new approaches to the treatment of chemical equilibria, which, brilliantly presented, are to be found scattered throughout the first edition of Ostwald’s "Lehrbuch der Allgemeinen Chemie" (Textbook of general chemistry). So there arose in 1889 the osmotic theory of galvanic current generation, which has not been seriously challenged since it was put forward more than thirty years ago and has undergone no appreciable elaboration since its acceptance, surely a clear sign that it has so far satisfied scientific needs. ..</br></br>The osmotic theory of current generation stipulates moreover that when a metal ion concentration is higher than consistent with the solution tension of the particular metal, on immersion of the metal, ions of the relevant metal electrode must go into solution, while conversely they must settle on the electrode when the reverse is the case.he electrode when the reverse is the case.)
  • Estabrook 1967 Methods Enzymol  + (.. The convenience and simplicity of the p.. The convenience and simplicity of the polarographic 'oxygen electrode' technique for measuring rapid changes in the rate of oxygen utilization by cellular and subcellular systems is now leading to its more general application in many laboratories. The types and design of oxygen electrodes vary, depending on the invetigator's ingenuity and specific requirements of the system under investigation.rements of the system under investigation.)
  • Gnaiger 1997 Transplant Proc  + (0RGAN PRESERVATION under hypothermic ische0RGAN PRESERVATION under hypothermic ischemia is enhanced by storage solutions that protect the vascular endothelium from ischemia-reperfusion injury. Ischemia-reperfusion injury leads to primary graft failure and chronic rejection, and is commonly assessed by measuring endothelial activation and damage of the endothelial plasma membrane. However, corresponding primary intracellular events are little understood compared with the secondary cytokine/adhesion molecule cascade and inflammatory responses.<sup>1, 2</sup> Because protection of intracellular and cell membrane function is fundamental for further improvement of organ preservation, we developed highresolution respirometry as a sensitive diagnostic test for mitochondrial and plasma membrane competence.<sup>3</sup> Whereas the plasma membrane remained impermeable after clinically relevant cold storage times of 8 hours and 20 to 60 minutes of reoxygenation, mitochondrial function was impaired at several steps of the respiratory chain.l function was impaired at several steps of the respiratory chain.)
  • Majiene 2019 Nutrients  + (1,4-naphthoquinones, especially juglone, a1,4-naphthoquinones, especially juglone, are known for their anticancer activity. However, plumbagin, lawsone, and menadione have been less investigated for these properties. Therefore, we aimed to determine the effects of plumbagin, lawsone, and menadione on C6 glioblastoma cell viability, ROS production, and mitochondrial function.</br></br>Cell viability was assessed spectrophotometrically using metabolic activity method, and by fluorescent Hoechst/propidium iodide nuclear staining. ROS generation was measured fluorometrically using DCFH-DA. Oxygen uptake rates were recorded by the high-resolution respirometer Oxygraph-2k.</br></br>Plumbagin and menadione displayed highly cytotoxic activity on C6 cells (IC<sub>50</sub> is 7.7 ± 0.28 μM and 9.6 ± 0.75 μM, respectively) and caused cell death by necrosis. Additionally, they increased the amount of intracellular ROS in a concentration-dependent manner. Moreover, even at very small concentrations (1-3 µM), these compounds significantly uncoupled mitochondrial oxidation from phosphorylation impairing energy production in cells. Lawsone had significantly lower viability decreasing and mitochondria-uncoupling effect, and exerted strong antioxidant activity.</br></br>Plumbagin and menadione exhibit strong prooxidant, mitochondrial oxidative phosphorylation uncoupling and cytotoxic activity. In contrast, lawsone demonstrates a moderate effect on C6 cell viability and mitochondrial functions, and possesses strong antioxidant properties.unctions, and possesses strong antioxidant properties.)
  • Leyssens 1996 J Physiol  + (1. As ATP has a higher affinity for Mg2+ t1. As ATP has a higher affinity for Mg2+ than ADP, the cytosolic magnesium concentration rises upon ATP hydrolysis. We have therefore used the Mg(2+)-sensitive fluorescent indicator Magnesium Green (MgG) to provide an index of changing ATP concentration in single rat cardiomyocytes in response to altered mitochondrial state. 2. In response to FCCP, [Mg2+]i rose towards a plateau coincident with the progression to rigor, which signals ATP depletion. Contamination of the MgG signal by changes in intracellular free Ca2+ concentration (the KD of MgG for Ca2+ is 4.7 microM) was excluded by simultaneous measurement of [Ca2+]i and [Mg2+]i in cells dual loaded with fura-2 and MgG. The response to FCCP was independent of external Mg2+, confirming an intracellular source for the rise in [Mg2+]i. 3. Simultaneous measurements of mitochondrial NAD(P)H autofluorescence and mitochondrial potential (delta psi m; .-1 fluorescence) and of autofluorescence and MgG allowed closer study of the relationship between [Mg2+]i and mitochondrial state. Oligomycin abolished the FCCP-induced rise in [Mg2+]i without altering the change in autofluorescence. Thus, the rise in [Mg2+]i in response to FCCP is consistent with the release of intracellular Mg2+ following ATP hydrolysis by the mitochondrial F1F0-ATPase. 4. The rise in [Mg2+]i was correlated with cell-attached recordings of ATP-sensitive K+ channel (KATP) activity. In response to FCCP, an increase in KATP channel activity was seen only as [Mg2+]i reached a plateau. In response to blockade of mitochondrial respiration and glycolysis with cyanide (CN-) and 2-deoxyglucose (DOG), [Mg2+]i rose more slowly but again KATP channel opening increased only when [Mg2+]i reached a plateau and the cells shortened. 5. Oligomycin decreased the rate of rise of [Mg2+]i delayed the onset of rigor and increased the rate of mitochondrial depolarization in response to CN-_DOG. Thus, with blockade of mitochondrial respiration delta psi m is maintained by the mitochondrial F1F0-ATPase at the expense of ATP reserves. 6. In response to CN-_DOG, the initial rise in [Mg2+]i was accompanied by a small rise in [Ca2+]i. After [Mg2+]i reached a plateau and rigor developed, [Ca2+]i rose progressively. On reperfusion, in hypercontracted cells, [Ca2+]i recovered before [Mg2+]i and [ca2+]i oscillations were sustained while [Mg2+]i decreased. Thus on reperfusion, full recovery of [ATP]i is slow, but the activation of contractile elements and the restoration of [Ca2+]i does not require the re-establishment of millimolar concentrations of ATP.hment of millimolar concentrations of ATP.)
  • Satoh 1995 Br J Pharmacol  + (1. Effects of 3-hydroxy-3-methylglutaryl c1. Effects of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, pravastatin and simvastatin, on the myocardial level of coenzyme Q10, and on mitochondrial respiration were examined in dogs. 2. Either vehicle (control), pravastatin (4 mg kg-1 day-1), or simvastatin (2 mg kg-1 day-1) was administered orally for 3 weeks. First, the myocardial tissue level of coenzyme Q10 was determined in the 3 groups. Second, ischaemia was induced by ligating the left anterior descending coronary artery (LAD) in anaesthetized open chest dogs, pretreated with the inhibitors. After 30 min of ischaemia, nonischaemic and ischaemic myocardium were removed from the left circumflex and LAD regions, respectively, and immediately used for isolation of mitochondria. The mitochondrial respiration was determined by polarography, with glutamate and succinate used as substrates. 3. Simvastatin significantly decreased the myocardial level of coenzyme Q10, but pravastatin did not. 4. Ischaemia decreased the mitochondrial respiratory control index (RCI) in both groups. Significant differences in RCI between nonischaemic and ischaemic myocardium were observed in the control and simvastatin-treated groups. 5. Only in the simvastatin-treated group did ischaemia significantly decrease the ADP/O ratio, determined with succinate. 6. The present results indicate that simvastatin but not pravastatin may cause worsening of the myocardial mitochondrial respiration during ischaemia, probably because of reduction of the myocardial coenzyme Q10 level.tion of the myocardial coenzyme Q10 level.)
  • Chance 1962 J Biol Chem  + (1. In succinate oxidation reactivated by a1. In succinate oxidation reactivated by a low concentration of adenosine triphosphate, addition of small amounts of adenosine diphosphatc will lead to reestablishment of the inhibited state of succinate oxidation after a short burst of respiration.</br></br>2. The inhibited state is not relieved by either phosphate or phosphate acceptors. </br></br>3. The inhibition is closely correlated with a high degree of oxidation of mitochondrial reduced diphosphopyridine nucleotide, which occurs immediately on addition of adenosine diphosphate and is followed by the inhibition of succinate oxidation after the oxidation or rather small amounts of succinate. </br></br>4. Oxidation of more than approximately two-thirds of the total diphosphopyridinc nuclcotide (DPN) reducible by succinate and adenosine triphosphate eventually leads to inhibition of succinate oxidation. </br></br>5. Based on independent evidence for a compartmentation of mitochondrial pyridine nucleotide (approximately one-third available to DPN-linked substrates), it is proposed that inhibi- tion occurs when oxidation of DPN in the compartment available to malate causes oxaloacetate formation sufficient to inhibit succinate oxidation. </br></br>6. The general possibility of DPN control of malate oxidation is considered with respect to the whole question of oxaloacetate regulation of the citric acid cycle.etate regulation of the citric acid cycle.)
  • Hatefi 1962 J Biol Chem-XLII  + (1. It has been shown that the electron tra1. It has been shown that the electron transfer system in beef heart mitochondria may be reconstituted either totally or in any desired sequential segment by appropriate combinations of two or more of the four primary complexes that have been isolated in highly purified form in this laboratory. </br></br>2. The four enzyme systems that collectively comprise the complete machinery for transfer of electrons from reduced diphosphopyridine nucleotide (DPNH; =NADH) and succinate to oxygen re: I, DPNH-coenzyme Q reductase; II, succinic-coenzyme Q reductase; III, QH2-cytochrome ''c'' reductase; and IV, cytochrome ''c'' reductase. The specific inhibitors of each complex have been studied. </br></br>3. By appropriate combinations of the primary complexes the following secondary activities have been reconstituted: V, DPNH-cytochrome ''c'' reductase; VI, succinic-cytochrome ''c'' reductase; VII, DPNH, succinic-cytochrome c reductase; VIII, DPNH oxidase; IX, succinic oxidase; and X, DPNH, succinic oxidase activity. The general oxidation-reduction properties of the reconstituted systems, both in the presence and the absence of the usual specific inhibitors of the electron transfer system, are essentially the same as those found for the same activities in the intact mitochondria and in the integrated particles derived therefrom. </br></br>4. The reconstituted activities are quite stable to repeated freezing, thawing, and storage at -2O °C, and for the most part, when once formed, are not dissociated by dilution of the mixture or by centrifugation. The evidence supporting the conclusion that reconstitution necessarily involves a particle-particle interaction is discussed.article-particle interaction is discussed.)
  • Opalka 2004 Br Poult Sci  + (1. M. iliotibialis (MIT) and M. pectoralis1. M. iliotibialis (MIT) and M. pectoralis (MP) of the BUT Big 6 and Kelly BBB turkey were characterised with respect to physical properties, mitochondrial function, metabolic state, morphology and meat quality.</br></br>2. Mitochondrial enzyme activity and respiration rates in MP declined with increasing age while glycolytic enzyme activity remained nearly constant.</br></br>3. There were no major differences between BUT Big 6 and Kelly BBB with respect to histological, histochemical or biochemical variables. In spite of the greater adult weight of BUT Big 6, body proportion was equal in both strains.</br></br>4. In agreement with the histochemical findings MIT showed higher oxidative capacities, while glycolytic enzyme activity was higher in MP.</br></br>5. Pyruvate was the best substrate for oxidative phosphorylation in MIT, but not in MP. Pyruvate dehydrogenase (PDH) activity was up to 15 times less in MP and blood lactate was correlated with intramuscular pH.</br></br>6. Turkey breast muscle was restricted in its ability to oxidise pyruvate, especially in those animals that tended to develop intramuscular acidosis post mortem.</br></br>7. It is concluded that the ''in vivo'' metabolic environment results in acidosis and impaired meat quality, at least in turkey M. pectoralis.quality, at least in turkey M. pectoralis.)
  • Claude 1946 J Exp Med  + (1. Materials and technical procedures invo1. Materials and technical procedures involved in the preparation of liver suspensions have been described and discussed. </br>2. Liver extracts prepared by the present method appear to contain almost exclusively elements of cytoplasmic origin and can be considered to represent, on a large scale, the cytoplasm of liver cells.large scale, the cytoplasm of liver cells.)
  • Wilson 1970 Biochim Biophys Acta  + (1. Oxidation of NADH by fumarate coupled t1. Oxidation of NADH by fumarate coupled to synthesis of ATP was found to occur in cyanide-poisoned rat heart submitochondrial particles. The reaction was inhibited by amytal, thenoyltrifluoroacetone and malonate, indicating the involvement of a portion of the electron transfer chain.</br></br>2. Cytochrome b became oxidized (while the other cytochromes remained reduced) during the oxidation of NADH by fumarate, suggesting that cytochrome b is part of the reaction pathway.</br></br>3. Succinate was recovered as the reaction product and accounted for the NADH oxidized.</br></br>4. The P/2e ratios indicate that one ATP was produced for each pair of electrons transferred to fumarate.</br></br>5. The reaction was also demonstrated to be present in liver and gastrocnemius muscle of rat. The reaction rate in heart was 2.0 times that of gastrocnemius and 3.3 times that of liver. These differences are not related to the activities of NADH or succinate dehydrogenase.</br></br>6. The ubiquitous nature of this reaction suggests that it could serve as an important physiological mechanism for generating extra glycolytic energy during periods of anoxia.lycolytic energy during periods of anoxia.)
  • Boveris 1973 Biochem J  + (1. Pigeon heart mitochondria produce H(2)O1. Pigeon heart mitochondria produce H(2)O(2) at a maximal rate of about 20 nmol/min per mg of protein. </br></br>2. Succinate-glutamate and malate-glutamate are substrates which are able to support maximal H(2)O(2) production rates. With malate-glutamate, H(2)O(2) formation is sensitive to rotenone. Endogenous substrate, octanoate, stearoyl-CoA and palmitoyl-carnitine are by far less efficient substrates. </br></br>3. Antimycin A exerts a very pronounced effect in enhancing H(2)O(2) production in pigeon heart mitochondria; 0.26 nmol of antimycin A/mg of protein and the addition of an uncoupler are required for maximal H(2)O(2) formation. </br></br>4. In the presence of endogenous substrate and of antimycin A, ATP decreases and uncoupler restores the rates of H(2)O(2) formation. </br></br>5. Reincorporation of ubiquinone-10 and ubiquinone-3 to ubiquinone-depleted pigeon heart mitochondria gives a system in which H(2)O(2) production is linearly related to the incorporated ubiquinone. </br></br>6. The generation of H(2)O(2) by pigeon heart mitochondria in the presence of succinate-glutamate and in metabolic [[State 4]] has an optimum pH value of 7.5. In States 1 and 3u, and in the presence of antimycin A and uncoupler, the optimum pH value is shifted towards more alkaline values. </br></br>7. With increase of the partial pressure of O(2) to the hyperbaric region the formation of H(2)O(2) is markedly increased in pigeon heart mitochondria and in rat liver mitochondria. With rat liver mitochondria and succinate as substrate in State 4, an increase in the ''p''O(2) up to 1.97 MPa (19.5 atm) increases H(2)O(2) formation 10-15-fold. Similar ''p''O(2) profiles were observed when rat liver mitochondria were supplemented either with antimycin A or with antimycin A and uncoupler. No saturation of the system with O(2) was observed up to 1.97 MPa (19.5 atm). By increasing the ''p''O(2) to 1.97 MPa (19.5atm), H(2)O(2) formation in pigeon heart mitochondria with succinate as substrate increased fourfold in metabolic State 4, with antimycin A added the increase was threefold and with antimycin A and uncoupler it was 2.5-fold. In the last two saturation of the system with oxygen was observed, with an apparent ''K''(m) of about 71 kPa (0.7-0.8 atm) and a ''V''(max) of 12 and 20 nmol of H(2)O(2)/min per mg of protein. </br></br>8. It is postulated that in addition to the well-known flavin reaction, formation of H(2)O(2) may be due to interaction with an energy-dependent component of the respiratory chain at the cytochrome ''b'' level.atory chain at the cytochrome ''b'' level.)
  • Mitchell 1967 Biochem J  + (1. Pulses of acidity of the outer aqueous 1. Pulses of acidity of the outer aqueous phase of rat liver mitochondrial suspensions induced by pulses of respiration are due to the translocation of H(+) (or OH(-)) ions across the osmotic barrier (M phase) of the cristae membrane and cannot be attributed to the formation (with acid production) of a chemical intermediate that subsequently decomposes. 2. The effective quantity of protons translocated per bivalent reducing equivalent passing through the succinate-oxidizing and beta-hydroxybutyrate-oxidizing spans of the respiratory chain are very close to 4 and 6 respectively. These quotients are constant between pH5.5 and 8.5 and are independent of changes in the ionic composition of the mitochondrial suspension medium provided that the conditions permit the accurate experimental measurement of the proton translocation. 3. Apparent changes in the -->H(+)/O quotients may be induced by conditions preventing the occurrence of the usual backlash; these apparent changes of -->H(+)/O are attributable to a very fast electrically driven component of the decay of the acid pulses that is not included in the experimental extrapolations. 4. Apparent changes in the -->H(+)/O quotients may also be induced by the presence of anions, such as succinate, malonate and phosphate, or by cations such as Na(+). These apparent changes of -->H(+)/O are due to an increase in the rate of the pH-driven decay of the acid pulses. 5. The uncoupling agents, 2,4-dinitrophenol, carbonyl cyanide p-trifluoromethoxyphenylhydrazone and gramicidin increase the effective proton conductance of the M phase and thus increase the rate of decay of the respiration-driven acid pulses, but do not change the initial -->H(+)/O quotients. The increase in effective proton conductance of the M phase caused by these uncouplers accounts quantitatively for their uncoupling action; and the fact that the initial -->H(+)/O quotients are unchanged shows that uncoupler-sensitive chemical intermediates do not exist between the respiratory-chain system and the effective proton-translocating mechanism. 6. Stoicheiometric acid-base changes associated with the activity of the regions of the respiratory chain on the oxygen side of the rotenone- and antimycin A-sensitive sites gives experimental support for a suggested configuration of loop 3.xperimental support for a suggested configuration of loop 3.)
  • Claude 1944 J Exp Med  + (1. Rat tumor extracts, containing chiefly 1. Rat tumor extracts, containing chiefly the cytoplasmic constituents of leukemic cells, were fractionated into three main portions, the different components separating in the centrifuge according to size. 2. Mitochondria were isolated by centrifugation at relatively low speed. Elementary composition of purified mitochondria was found to correspond to about 11.5 per cent nitrogen, 1.6 per cent phosphorus, and 27 per cent lipids. Phosphorus and nitrogen content of the lipid portion suggests that as much as 75 to 80 per cent of the lipids of mitochondria is represented by phospholipids. Tests for ribose nucleic acid were positive. 3. Microsomes were separated by means of centrifugation at 18,000 x g. A relation between the high phosphorus content of the microsomes and the marked basophilia of the cytoplasm of leukemic cells is suggested. 4. Phosphorus distribution in the tumor extract, and light absorption analysis of the third fraction, seem to demonstrate that nucleic acid was not present either in a free condition, or in the form of nucleoprotein of relatively low molecular weight. The nature of the results suggests that ribose nucleic acid occurs in the cytoplasm of leukemic cells only in association with formed elements of relatively large size, namely microsomes, and mitochondria.size, namely microsomes, and mitochondria.)
  • Ernster 1969 Eur J Biochem  + (1. Submitochondrial particles were prepare1. Submitochondrial particles were prepared from beef‐heart mitochondria by sonication in the presence of EDTA. The particles were lyophilized and repeatedly extracted with pentane until no ubiquinone was found in the extract. Treatment of the ubiquinone‐depleted particles with pentane containing a suitable concentration of ubiquinone (ubiquinone‐50) and subsequent quick washing with ubiquinone‐free pentane resulted in a “re‐incorporation” of ubiquinone in an amount similar to that present in the original particles (3–6 nmoles/mg protein).</br></br>2. The ubiquinone‐depleted particles exhibited very low or no succinate and NADH oxidase activities, which were restored upon the re‐incorporation of ubiquinone to the levels found in the lyophilized particles before extraction with pentane. Partial (about 50 %) extraction of ubiquinone resulted in markedly decreased succinate and NADH oxidase activities.</br></br>3. Added cytochrome ''c'' did not replace ubiquinone in restoring the succinate or NADH oxidase activity of ubiquinone‐depleted particles. It stimulated the NADH oxidase, but not the succinate oxidase, activity of the “ubiquinone‐incorporated” particles, but the same stimulation occurred with the lyophilized particles before ubiquinone extraction. The normal, lyophilized, and “ubiquinone‐incorporated” particles contained equal amounts of both total and enzymatically reducible cytochromes.</br></br>4. In the presence of KCN, NADH reduced the cytochromes, including cytochrome ''b'', only at insignificant rates in the ubiquinone‐depleted particles as compared to the normal and lyophilized preparations, and these rates were greatly stimulated upon the re‐incorporation of ubiquinone. Succinate caused a rapid partial (about 25 %) reduction of cytochrome ''b'', but not of the rest of the cytochromes, in the ubiquinone‐depleted particles. This reduction occurred also in the absence of KCN, and the fraction of cytochrome ''b'', so reduced was not reoxidized when succinate oxidation was inhibited by malonate. Evidence for the occurrence of such an enzymatically non‐oxidizable form of cytochrome ''b'' was also obtained in the normal, lyophilized and “ubiquinone‐incorporated” particles, but, in those cases, this cytochrome ''b'' was reduced by both succinate and NADH. In the presence of antimycin A, all cytochrome ''b'' in the ubiquinone‐depleted particles was rapidly reduced by succinate but not by NADH.</br></br>5. The normal and lyophilized particles catalyzed a rotenone‐sensitive oxidation of NADH by fumarate. This reaction was completely absent from the ubiquinone‐depleted particles and was restored upon the re‐incorporation of ubiquinone.</br></br>6. N,N,N′,N′‐Tetramethyl‐p‐phenylenediamine catalyzed an NADH and succinate oxidase activity in antimycin A‐inhibited particles. This NADH oxidase activity was partially sensitive to rotenone in the normal, lyophilized and “ubiquinone‐incorporated” particles, but completely rotenone‐insensitive in the ubiquinone‐depleted particles. All four types of particles were active in catalyzing the antimycin A‐sensitive oxidation of menadiol.</br></br>7. It is concluded that uniquinone is essential for the interaction of succinate dehydrogenase, NADH dehydrogenase and cytochrome ''b'', and that this interaction is a requisite for the normal function of the respiratory chain. Functionally modified forms of cytochrome ''b'', arising as a consequence of structural damage or antimycin A treatment, are discussed in relation to existing information and proposals concerning the role of cytochrome ''b'' and ubiquinone in electron transport.'b'' and ubiquinone in electron transport.)
  • Henderson 1969 Biochem J  + (1. The action of the antibiotics enniatin 1. The action of the antibiotics enniatin A, valinomycin, the actin homologues, gramicidin, nigericin and dianemycin on mitochondria, erythrocytes and smectic mesophases of lecithin-dicetyl hydrogen phosphate was studied. 2. These antibiotics induced permeability to alkali-metal cations on all three membrane systems. 3. The ion specificity on each membrane system was the same. 4. Enniatin A, valinomycin and the actins did not induce permeability to protons, whereas nigericin and dianemycin rendered all three membrane systems freely permeable to protons. 5. Several differences were noted between permeability induced by nigericin and that induced by gramicidin. 6. The action of all these antibiotics on mitochondrial respiration could be accounted for by changes in passive ion permeability of the mitochondrial membrane similar to those induced in erythrocytes and phospholipid membranes, if it is assumed that a membrane potential is present in respiring mitochondria.tial is present in respiring mitochondria.)
  • Harafuji 1980 J Biochem  + (1. The apparent binding constant (Kapp(Ca-1. The apparent binding constant (Kapp(Ca-G)) for GEDTA (ethylene glycol bis(β-aminoethyl ether)-N, N, N', N'-tetraacetic acid, EGTA) to calcium was determined under conditions of biological significance in the presence of various kinds of pH-buffering agents, using murexide or tetramethylmurexide as a Ca indicator.</br>2. The value of Kapp(Ca-G) at pH 6.80 was 1.0×106M-1 at an ionic strength of 0.114 at 20°C, irrespective of the type of pH-buffering ions. This value is similar to that of Allen, Blinks and Prendergast (1977) (Science 196, 996-998), but still half that calculated from the results of Schwarzenbach, Senn and Anderegg (1957) (Helv. Chim. Acta 40, 1886-1900).</br>3. The value of Kapp(Ca-G) varied according to the following equation as the ionic strength (I) was varied from 0.039 to 0.264:</br>log Kapp(Ca-G)=6.460-[2_??_I/(1+_??_I)-0.4×I] (pH 6.80, 20°C)</br>4. The discrepancy between the present results and previous ones (Ogawa, Y. (1968) J. Biochem. 64, 255-257) may have been due to inadequate regulation of the temperature of the reaction medium in the previous determinations, during which an increase in the temperature of the solution may have occurred.</br>An increase of temperature causes a decrease in the pH of the solution in the presence of histidine, imidazole or Tris-maleate, but causes very little change of pH in the presence of phosphate or maleate.</br>5. The association rate constant for GEDTA with calcium was determined by the stoppedflow method in solutions containing 100mM KCl and 20mM pH-buffering ions at 20°C: the values obtained were 1.4×106M-1s-1 in the presence of MOPS-KOH at pH 6.80; 3.0×106M-1s-1 with imidazole at pH 6.80; 1.0×106M-1s-1 with Tris-maleate at pH 6.80..0×106M-1s-1 with Tris-maleate at pH 6.80.)
  • Harris 1968 Biochem J  + (1. The concentration-dependence of the int1. The concentration-dependence of the intramitochondrial accumulation of l-malate and succinate was measured and expressed in the form of adsorption isotherms. The accumulation, however, may arise because of an internal positive potential. 2. The competition for accumulation offered by some other anions, including phosphate, was measured and is expressed conventionally by additional terms in the adsorption equation. 3. The interactions between anions were also studied when one was acting as oxidized substrate. 4. In some examples there is a parallel between the effects of an added anion on both accumulation and oxidation; in other cases chemical participation of the added substance in metabolism is presumed to remove the correlation. 5. It is suggested that by combining kinetic data on penetration with stoicheiometric data on accumulation and specific reaction rates it may be possible to account for the rates of respiration obtained with intact mitochondria. 6. It is possible to show that there is a certain phosphate/substrate ratio for maximum phosphorylation rate with some substrates. This is to be expected when phosphate and substrate compete for accumulation.te and substrate compete for accumulation.)
  • Koenig 1969 Biochem J  + (1. The effects of succinate oxidation on p1. The effects of succinate oxidation on pyruvate and also isocitrate oxidation by rat liver mitochondria were studied. 2. Succinate oxidation was without effect on pyruvate and isocitrate oxidation when respiration was maximally activated with ADP. 3. When respiration was partially inhibited by atractylate, succinate oxidation severely inhibited the oxidation of pyruvate and isocitrate. 4. This inhibitory effect of succinate was associated with a two- to three-fold increase in the reduction of mitochondrial NAD(+) but no change in the reduction of cytochrome b. 5. It is concluded that, in the partially energy-controlled state, respiration is more severely inhibited at the first phosphorylating site than at the other two. 6. The effects of succinate oxidation are compared with those of palmitoylcarnitine oxidation. It is concluded that a rapid flow of electrons directly into the respiratory chain at the level of cytochrome b is in itself inadequate to inhibit the oxidation of intramitochondrial NADH. 7. The effects of succinate oxidation on pyruvate oxidation were similar in rat heart and liver mitochondria.milar in rat heart and liver mitochondria.)
  • Hoek 1970 Biochim Biophys Acta  + (1. The kinetics of the efflux of Pi and ma1. The kinetics of the efflux of Pi and malate as well as the relationship between Pi transport and intra- and extramitochondrial pH changes were studied in rat-liver mitochondria in the presence of rotenone and oligomycin at different pH's.</br></br>2. At high pH a fast efflux of Pi from the mitochondria occurs in the first few seconds, followed by a slow re-entry of Pi into the mitochondria. Under the same conditions the exit of malate shows a time lag of 2–4 sec. The exit of malate coincides with the re-entry of Pi.</br></br>3. In the presence of butylmalonate the exit of endogenous Pi is coupled with a concomitant alkalinization of the mitochondrial matrix space, as calculated from the distribution of 5,5-[14C]dimethyloxazolidine-2,4-dione.</br></br>4. The stoicheiometry of the Pi-hydroxyl exchange was found to be 1:1.</br></br>5. The kinetics of Pi transport are consistent with previous observations that there is a direct exchange between OH− and Pi, but not between OH− and malate. The equilibrium distribution of H2PO4− and OH− deviates from the Donnan distribution. This may be explained by assuming a pH-dependent binding of Pi in the mitochondria.pendent binding of Pi in the mitochondria.)
  • Claude 1945 J Exp Med  + (1. The present paper constitutes a prelimi1. The present paper constitutes a preliminary study of the morphology of mitochondria by means of electron microscopy.</br></br>2. The mitochondria that were the subject of this investigation were obtained from a lymphosarcoma of the rat. They were separated from the other components of the leukemic cells by a method of differential centrifugation, and thus made available for direct examination in the electron microscope.</br></br>3. In the purified form the mitochondria appeared as spherical bodies, the majority of them varying in size approximately from 0.6 to 1.3 µ in diameter.</br></br>4. Certain aspects of mitochondria in the electron microscope suggest that these elements are surrounded by a differentiated membrane. In some cases the limiting membrane seemed to be responsible for maintaining the general shape of the mitochondria, even when most of the mitochondrial substance had been lost.</br></br>5. By means of the electron microscope, it is possible to distinguish small elements, 80 to 100 mµ in diameter, within the body of certain mitochondria. Further work is suggested to establish whether these small granules are normal constituents of mitochondria, and what relation may exist between them and ordinary microsomes.</br></br>6. The nature of mitochondria as morphological units is discussed. Present evidence indicates that mitochondria constitute definite physical entities which can persist in the absence of the cytoplasm.n persist in the absence of the cytoplasm.)
  • Griffiths 1995 Biochem J  + (1. The yield of mitochondria isolated from1. The yield of mitochondria isolated from perfused hearts subjected to 30 min ischaemia followed by 15 min reperfusion was significantly less than that for control hearts, and this was associated with a decrease in the rates of ADP-stimulated respiration. 2. The presence of 0.2 microM cyclosporin A (CsA) in the perfusion medium during ischaemia and reperfusion caused mitochondrial recovery to return to control values, but did not reverse the inhibition of respiration. 3. A technique has been devised to investigate whether the Ca(2+)-induced non-specific pore of the mitochondrial inner membrane opens during ischaemia and/or reperfusion of the isolated rat heart. The protocol involved loading the heart with 2-deoxy[3H]glucose ([3H]DOG), which will only enter mitochondria when the pore opens. Subsequent isolation of mitochondria demonstrated that [3H]DOG did not enter mitochondria during global isothermic ischaemia, but did enter during the reperfusion period. 4. The amount of [3H]DOG that entered mitochondria increased with the time of ischaemia, and reached a maximal value after 30-40 min of ischaemia. 5. CsA at 0.2 microM did not prevent [3H]DOG becoming associated with the mitochondria, but rather increased it; this was despite CsA having a protective effect on heart function similar to that shown previously [Griffiths and Halestrap (1993) J. Mol. Cell. Cardiol. 25, 1461-1469]. 6. The non-immunosuppressive CsA analogue [MeAla6]cyclosporin was shown to have a similar Ki to CsA on purified mitochondrial peptidyl-prolyl cis-trans-isomerase and mitochondrial pore opening, and also to have a similar protective effect against reperfusion injury. 7. Using isolated heart mitochondria, it was demonstrated that pore opening could become CsA-insensitive under conditions of adenine nucleotide depletion and high matrix [Ca2+] such as may occur during the initial phase of reperfusion. The apparent increase in mitochondrial [3H]DOG in the CsA-perfused hearts is explained by the ability of the drug to stabilize pore closure and so decrease the loss of [3H]DOG from the mitochondria during their preparation.the mitochondria during their preparation.)
  • Kearney 1960 J Biol Chem  + (1. Unlike other known flavoproteins, in wh1. Unlike other known flavoproteins, in which the flavin is relatively loosely bound and is easily liberated by suitable methods of denaturation, in succinic dehydrogenase from beef heart the flavin component is so tightly held that neither treatment with strong acids nor thermal denaturation separates it from the protein.</br></br>2. Extensive digestion of the purified dehydrogenase with suitable proteolytic enzymes liberates the flavin in an acid-soluble form, which is not, however, identical with known derivatives of riboflavin. The flavin appears in the digest in several chromatographically distinct forms, which may be separated from each other by purification on ion exchange resins or by chromatography on filter paper.</br></br>3. The main flavin components have been extensively purified and degraded to the mononucleotide and dephosphorylated flavin levels. The dinucleotide contains 1 mole of 5’-adenylic acid, 2 atoms of phosphorus bound in pyrophosphate linkage and 1 mole of ribose. It differs from authentic flavin adenine dinucleotide (FAD) in numerous regards, including its inactivity in the n-amino acid oxidase test, shifted absorption spectrum, shifted pH-fluorescence curve, and in the presence of cationic group(s). After degradation to the mononucleotide and dephosphorylated flavin level, similar differences exist between the resulting compounds and authentic riboflavin 5’-phosphate and riboflavin, respectively. Irradiation in alkali degrades the flavin further, but the resulting compound is not identical with lumiflavin.</br></br>4. These differences and the greater water solubility of the unphosphorylated compound as compared with riboflavin are best explained by the hypothesis that the flavin in the dehydrogenase is held to a peptide chain by a covalent linkage which survives proteolytic digestion. The compounds in the digest, therefore, would be peptides of FAD, representing fragments of the original enzyme.</br></br>5. Evidence for the flavin peptide hypothesis has come from the finding that throughout very extensive purification by a variety of methods the flavin is always accompanied by peptide material. In the most purified fraction, believed to be free of contaminating peptides, alanine, serine, threonine, glutamic acid, and valine were present in molar ratio to the flavin and an additional mole of serine was present as N-terminal group. Similar amino acid compositions were found in 2 other samples, purified by different procedures.</br></br>6. Evidence pertaining to the flavin peptide hypothesis and the possible structure of the flavin is discussed.ible structure of the flavin is discussed.)
  • Gnaiger 2013 Abstract MiP2013  + (10 years ago the uncoupling hypothesis was10 years ago the uncoupling hypothesis was presented for mitochondrial haplogroups of arctic populations suggesting that lower coupling of mitochondrial respiration to ATP production was selected for in favor of higher heat dissipation as an adaptation to cold climates [1,2]. Up to date no actual tests have been published to compare mitochondrial coupling in tissues obtained from human populations with regional mtDNA variations. Analysis of oxidative phosphorylation (OXPHOS) is a major component of mitochondrial phenotyping [3]. We studied mitochondrial coupling in small biopsies of arm and leg muscle of Inuit of the Thule and Dorset haplogroups in northern Greenland compared to Danes from western Europe haplogroups. Inuit had a higher capacity to oxidize fat substrate in leg and arm muscle, yet mitochondrial respiration compensating for proton leak was proportionate with OXPHOS capacity. Biochemical coupling efficiency was preserved across variations in muscle fiber type and uncoupling protein-3 content. After 42 days of skiing on the sea ice in northern Greenland, Danes demonstrated adaptive substrate control through an increase in fatty acid oxidation approaching the level of the Inuit, yet coupling control of oxidative phosphorylation was conserved. Our findings reveal that coupled ATP production is of primary evolutionary significance for muscle tissue independent of adaptations to the cold.ue independent of adaptations to the cold.)
  • ASMRM 2013 Seoul KR  + (10<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine - [http://asmrm2013.com/common_files/mess.asp ASMRM 2013], Seoul KR)
  • MiP2014  + (10<sup>th</sup> MiP''conference'': Joint IUBMB/MiP Symposium on Mitochondrial Physiology - a Point/Counterpoint Meeting, Obergurgl, Austria; with post-conference workshop '''[[MiPNet19.10 | 95th Oroboros O2k-Workshop]]'''.)
  • 10th Conference of the International Coenzyme Q10 Association 2022 Hamburg DE  + (10th Conference of the International Coenzyme Q10 Association, Hamburg, 2022)
  • 10th European Algae Industry Summit 2020 Reykjavik IS  + (10th European Algae Industry Summit, Reykjavik, Iceland, 2020)
  • 10th Int CeBiTec Research Conference 2021 Bielefeld DE  + (10th Int. CeBiTec Research Conference, Bielefeld, Germany, 2021)
  • 10th International Luebeck Conference on the Pathophysiology and Pharmacology of Erythropoietin and other Hemopoietic Growth Factors  + (10th International Luebeck Conference on the Pathophysiology and Pharmacology of Erythropoietin and other Hemopoietic Growth Factors, Lübeck, DE, [https://www.physio.uni-luebeck.de/index.php?id=162 10th International Luebeck Conference])
  • 10th Italian Meeting on Mitochondrial Disease 2020 IT  + (10th Italian Meeting on Mitochondrial Diseases , Virtual, 2020)
  • TriMAD Conference 2023 Pennsylvania US  + (10th Translational Research in Mitochondri10th Translational Research in Mitochondria/Metabolism, Aging, and Disease (TRiMAD) Conference, Pennsylvania, United States, 2023 </br></br></br></br>== General information ==</br>:::: TRiMAD is a collaborative venture between The Pennsylvania State University, University of Pittsburgh Medical Center, The Children’s Hospital of Philadelphia (CHoP) Research Institute, and The University of Pennsylvania Perelman School of Medicine ([https://www.huck.psu.edu/node/15830 Website])</br></br>== Venue == </br>:::: University of Pittsburgh</br>:::: Bridgeside Point 1, 5th Floor</br>:::: 100 Technology Drive</br>:::: Pittsburgh, PA 15219</br></br>== Organizers ==</br>:::: University of Pittsburgh</br>:::: Aging Institute</br>:::: Center for Metabolism & Mitochondrial Medicine</br></br>== Program ==</br>:::: Please find the programme [https://aging.pitt.edu/event/trimad-2023/ here]</br></br></br>== Registration ==</br>:::: [https://forms.office.com/pages/responsepage.aspx?id=ifT5nqDg606HzDpSYRL9DXg8U8hQ84RKssucFsBERrBURTU2T1lFR01DS0hYNlZGRjNDTzg2QVJRSC4u Register here]</br> </br>== Lecturers and tutors ==</br></br>:::: The list of speakers can be found [https://aging.pitt.edu/event/trimad-2023/ here]ttps://aging.pitt.edu/event/trimad-2023/ here])
  • Targeting Mitochondria World Congress 2019 Berlin DE  + (10th World Congress on Targeting Mitochond10th World Congress on Targeting Mitochondria, Berlin, Germany, 2019 </br></br></br>== General information == </br>:::: Flyer available for [http://wiki.oroboros.at/images/7/7f/Berlin_2019.pdf download]</br></br>== Venue == </br>:::: INTERCONINENTAL BERLIN HOTEL</br>:::: Budapester Str. 2, 10787</br>:::: Berlin, Germany</br>::::[https://targeting-mitochondria.com/venue Hotel and Travel]</br></br>== Programme ==</br>:::: [https://targeting-mitochondria.com/preliminary-program here]</br></br>== Speakers == </br>:::: List of speakers can be found [https://targeting-mitochondria.com/speakers-2019 here]</br></br>== Registration ==</br>:::: [https://targeting-mitochondria.com/registration Registration and more information]tration Registration and more information])
  • 115th International Titisee Conferences Titisee DE  + (115th ITC: Evolutionary mitochondrial biology: molecular, biochemical, and metabolic diversity, Titisee, Germany.)
  • 11th Annual Congress of Cardiology 2019 Suzhou CN  + (11th Annual Congress of Cardiology, Suzhou, China, 2019)
  • MiP2015  + (11th Conference on Mitochondrial Physiology, 2015 Sep 07-11, Luční Bouda, Czech Republic.)
  • Targeting Mitochondria World Congress 2020 Virtual  + (11th World Congress on Targeting Mitochond11th World Congress on Targeting Mitochondria, Virtual, 2020 </br></br></br>== General information == </br>:::: After a long and thorough discussion among the scientific and organizing committees, we have decided to organize our 11th Conference of Targeting Mitochondria, on October 29-30, 2020 as an ONLY Virtual Congress.</br></br>== Programme ==</br>:::: [https://targeting-mitochondria.com/preliminary-program here]</br></br>== Speakers == </br>:::: List of speakers can be found [https://targeting-mitochondria.com/speakers here]</br></br>== Registration ==</br>:::: [https://targeting-mitochondria.com/registration Registration and more information]tration Registration and more information])
  • 11th ÖGMBT Annual Meeting 2019 Salzburg AT  + (11th ÖGMBT Annual Meeting - Inside the world of biomolecules, Salzburg, Austria, 2019)
  • ASMRM 2015 Hangzhou CN  + (12<sup>th</sup> Conference of the Asian Society of Mitochondrial Research and Medicine - [http://www.ig.zju.edu.cn/ASMRM/EN/ ASMRM 2015], Hangzhou CN)
  • 12th International Conference on Obesity and Eating Disorders 2023 Vienna AT  + (12th International Conference on Obesity a12th International Conference on Obesity and Eating Disorders, Vienna, Austria, 2023 </br></br>== General Information == </br>:::: The theme of the conference is "New Emerging Challenges in Obesity and their Prevention"</br></br>== Venue ==</br>:::: [https://obesity.euroscicon.com/ How to get there]</br></br>== Program ==</br>:::: Program available [https://obesity.euroscicon.com/program-schedule here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://obesity.euroscicon.com/organizing-committee here]</br></br>== Registration ==</br>:::: [https://obesity.euroscicon.com/registration Registration and more information]</br>:::: Early registration deadline: 203-01-27</br>:::: Late registration deadline: 2023-04-10::: Late registration deadline: 2023-04-10)
  • IPC2021 Puerto Varas CL  + (12th International Phycological Congress -12th International Phycological Congress - IPC2021, Puerte Varas, Chile, 2021 </br></br>== Venue == </br>::::[https://ipc2021.com/logistic-information/ Venue and how to get there]</br></br>== Programme ==</br>:::: [https://ipc2021.com/scientific-program/ here]</br></br>== Speakers == </br>:::: List of speakers can be found [https://ipc2021.com/invited-speakers/ here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://ipc2021.com/local-organizing-committee-scientific-committee/ here]</br></br>== Registration ==</br>:::: [https://ipc2021.com/registration-and-registration-fees-submission-of-abstracts/ Registration and more information]tracts/ Registration and more information])
  • 12th ÖGMBT Annual Meeting 2020 Virtual Event  + (12th ÖGMBT Annual Meeting - Biomolecules in/for 21st century, Virtual Event, 2020 '''''- Conference will be held via a virtual interactive meeting. Oroboros Instruments will be present with a virtual booth.''''')
  • Life Sciences Meeting 2018 Innsbruck AT  + (13th Life Sciences Meeting, Innsbruck, Aus13th Life Sciences Meeting, Innsbruck, Austria, 2018 </br></br>__TOC__</br></br>== General information== </br>:::: The coming meeting will take place on the 5th and 6th of April, 2018 in the CCB (Center for Chemistry and Biomedicine) and offers all participants and young researchers the possibility to present their research work in the form of a posters or a short talk. At the end of the event the best presentation will be selected by a professional jury consisting of professors of the Medical University of Innsbruck and the winners will be awarded with a prize. The closure of the meeting will be made by the famous scientist Prof. Jannie Cracking of the Netherland Cancer Institute. The Medical University of Innsbruck is looking forward to welcoming Prof. Cracking as a „Key Note Speaker“. </br></br></br>== Venue == </br>:::: Center for Chemistry and Biomedicine (CCB)</br>:::: Innrain 80, 6020 Innsbruck</br>:::: [http://biocenter.i-med.ac.at/ Location]</br></br>== Organizers ==</br>:::: Medical University of Innsbruck</br></br>==Oroboros presentation ==</br>:::: TALK: Marie Skłodowska-Curie Project '''[[TRANSMIT]]''' [[Bastos Sant'Anna Silva AC|Bastos Sant'Anna Silva Ana Carolina]]: [[Bastos Sant'Anna Silva AC 2018 Life Sciences Meeting 2018 Innsbruck AT|Effect of cell-permeable succinate and malonate prodrugs on mitochondrial respiration in prostate cancer cells]]</br>:::: POSTER: Marie Skłodowska-Curie Project '''[[TRACT]]''' [[Chang Shao-Chiang]]: [[Chang 2018 Life Sciences Meeting 2018 Innsbruck AT|pH dependence of mitochondrial respiration and H<sub>2</sub>O<sub>2</sub> production in oral cancer cells – a pilot study.]]</br>:::: POSTER: K-Regio Project '''[[K-Regio_MitoFit|MitoFit]]''' [[Garcia-Souza LF|Garcia-Souza Luiz]]: [[Garcia-Souza 2018 Life Sciences Meeting 2018 Innsbruck AT|A respirometric cell viability test for peripheral-blood mononuclear cells and platelets]]-Souza 2018 Life Sciences Meeting 2018 Innsbruck AT|A respirometric cell viability test for peripheral-blood mononuclear cells and platelets]])
  • 13th Targeting Mitochondria Congress 2022 Berlin DE  + (13th Targeting Mitochondria Congress, Berlin, 2022)
  • EBSA2021 Vienna AT  + (13th congress of EBSA, Vienna, Austria, 2021)
  • FAOBMB 2015 Hyderabad IN  + (14<sup>th</sup> Congress of the Federation of Asian and Oceanian Biochemists and Molecular Biologists (FAOBMB) - [http://www.ccmb.res.in/faobmb2015/ FAOBMB 2015], Hyderabad IN)
  • EBSA 2023 Stockholm SE  + (14th congress of EBSA, Stockholm, Sweden, 2023)
  • The Power of Metabolism Linking energy supply and demand with contractile function 2017 Weimar DE  + (15th Annual Meeting: The Power of Metabolism - Linking energy supply and demand with contractile function, Weimar,)
  • ASMRM 2018 Busan KR  + (15th Conference of the Asian Society of Mitochondrial Research and Medicine, Busan, South Korea, 2018.)
  • 16th Chinese Biophysics Congress 2018 Chengdu CH  + (16th Chinese Biophysics Congress - Biophysics and human health , Chengdu, China, 2018)
  • J-mit 2017 Kyoto JP  + (17<sup>th</sup> Annual Conference of Janpanese Society of Mitochondrial Research and Medicine, Kyoto, Japan)
  • 17th Chinese Biophysics Congress 2019 Tianjin CN  + (17th Chinese Biophysics Congress, Tianjin , China, 2019)
  • 17th International Biochemistry of Exercise Conference 2018 Beijing CN  + (17th International Biochemistry of Exercise Conference, Beijing, China, 2018)
  • The 18th Annual Meeting of the Japan Mitochondrial Association 2018 Kurume JP  + (18th Annual Meeting of the Japan Mitochondrial Association, Kurume, 2018)
  • KSMRM2014  + (19<sup>th</sup> Annual Scientific Meeting of KSMRM , Seoul, Republic of Korea; [http://2014.ksmrm.org/congress/invitation.php KSMRM2014])
  • SHVM 2022 Seoul KR  + (19th Annual Meeting of the Society for Heart and Vascular Metabolism (SHVM), Seoul , South Korea, 2022)
  • 19th Beijing Conference and Exhibition on Instrumental Analysis 2021 Beijing CN  + (19th Beijing Conference and Exhibition on Instrumental Analysis, Beijing, China, 2021)
  • 19th Chinese Biophysics congress 2021 Anhui CN  + (19th Chinese Biophysics congress, Anhui Province, China, 2021)
  • ESP2021 Salzburg AT  + (19th Congress of the European Society for 19th Congress of the European Society for Photobiology - ESP2021, Salzburg, Austria, 2021 </br></br>== Venue == </br>:::: Faculty of Natural Sciences (NAWI) of the Paris Lodron University Salzburg (PLUS)</br>:::: Venue address: Hellbrunnerstrasse 34, 5020 Salzburg, Austria.</br>:::: [http://salzburg2021.photobiology.eu/congress-venue more information]</br></br>== Program ==</br>:::: [http://salzburg2021.photobiology.eu/ here]</br></br>== Speakers == </br>:::: List of speakers can be found [http://salzburg2021.photobiology.eu/ here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [http://salzburg2021.photobiology.eu/organizing-committee here]</br></br>== Registration ==</br>:::: [http://salzburg2021.photobiology.eu/ Registration and more information]ogy.eu/ Registration and more information])
  • Chlamy 2021 Ile des Embiez FR  + (19th International Conference on the Cell and Molecular Biology of Chlamydomonas, Ile des Embiez, France, 2021)
  • FEBS 2023 Luso PT  + (1<sup>st</sup> 1st FEBS Workshop “Redox Medicine Workshop, Luso, Portugal, 2023)
  • MiPschool Schroecken AT 2007  + (1<sup>st</sup> MiP''summer school'' on Mitochondrial Respiratory Physiology, 2007 July 12-18, Schroecken, AT.)
  • 1st Myocardial Function Symposium 2020 Graz AT  + (1st Myocardial Function Symposium: “Targets in cardiometabolic disease”, Graz, Austria, 2020)
  • SHVM 2021 Virtual  + (1st virtual meeting of the Society for Heart and Vascular Metabolism (SHVM), Virtual, 2021)
  • Goncalves 2017 J Cell Commun Signal  + (1α,25-Dihydroxyvitamin D<sub>3</s1α,25-Dihydroxyvitamin D<sub>3</sub> (1,25-D<sub>3</sub>) is critical for the maintenance of normal male reproduction since reduced fertility is observed in vitamin D-deficient rats. Gamma-glutamyl transpeptidase (GGT) is a membrane-bound enzyme that is localized on Sertoli cells and catalyses the transfer of the gamma-glutamyl residues to an amino acid or peptide acceptor. Sertoli cells are also responsible for providing nutrients, as lactate, to the development of germ cells. The aim of this study was to investigate the effect and the mechanism of action of 1,25-D<sub>3</sub> on GGT on Sertoli cell functions from 30-day-old immature rat testis. Results demonstrated that 1,25-D<sub>3</sub> stimulates GGT activity at Sertoli cells plasma membrane through a PKA-dependent mechanism of action, which was not dependent of active ''de novo'' protein synthesis. The hormone increases glucose uptake, as well as lactate production and release by Sertoli cells without altering the reactive oxygen species (ROS) generation. In addition, 1,25-D<sub>3</sub> did not change reduced glutathione (GSH) amount or oxygen consumption, and diminished Sertoli cell death. These findings demonstrate that 1,25-D<sub>3</sub> stimulatory effect on GGT activity, glucose uptake, LDH activity and lactate production seem to be an important contribution of Sertoli cells for germ cells nutrition and for a full and active ongoing spermatogenesis.mportant contribution of Sertoli cells for germ cells nutrition and for a full and active ongoing spermatogenesis.)
  • Royall 1993 Arch Biochem Biophys  + (2',7'-Dichlorofluorescein and dihydrorhoda2',7'-Dichlorofluorescein and dihydrorhodamine 123 were evaluated as probes for detecting changes in intracellular H2O2 in cultured endothelial cells. Stable intracellular levels of these probes were established within 15 min of exposure to the probe in culture medium. With continued presence of the probe in the medium, intracellular levels were unchanged for 1 h. However, if medium without the probes was used after intracellular loading had occurred, there was a greater than 90% loss of intracellular dichlorofluorescin, dichlorofluorescein, and dihydrorhodamine 123 while intracellular rhodamine 123 decreased by only 15%. Exposure of endothelial cells to exogenous 100 microM H2O2 for 1 h increased intracellular rhodamine 123 by 83%, but there was a reproducible decrease of 53% in intracellular dichlorofluorescein. Exposure to 0.05 mM BCNU plus 10 mM aminotriazole for 2 h increased intracellular rhodamine 123 by 111%. In vitro studies of dihydrorhodamine 123 oxidation were similar to previous reports of dichlorofluorescin oxidation. Oxidation of dihydrorhodamine 123 does not occur with H2O2 alone, but is mediated by a variety of secondary H2O2-dependent intracellular reactions including H2O2-cytochrome c and H2O2-Fe2+. Our results suggest that detection of increased oxidation of these probes in endothelial cells is most useful as a marker of a change in general cellular oxidant production.ge in general cellular oxidant production.)
  • Lardy 1953 J Biol Chem  + (2,4-Dinitrophenol greatly enhanced the 2,4-Dinitrophenol greatly enhanced the liberation of inorganic phosphate from ATP by the nuclear and mitochondrial fraction of rat liver. </br>The microsomal and supernatant fractions did not exhibit this effect. </br></br>With mitochondria (Mw) the rate of phosphate liberation was proportional to the DNP concentration up to 6 X 10-5 M In the presence of excess DNP the rate was proportional to the quantity of Mw nd to time. </br></br>With both fresh and preaged Mw, the response to DNP was much greater </br>in mediums containing salt (either NaCl or KCl) than in isotonic sucrose. Magnesium salts in appreciable concentrations depressed the response of fresh Mw to DNP, but enhanced the response in preaged Mw. Calcium salts, which activate ATP hydrolysis by fresh Mw in the absence of DNP, also depressed the effect of DNP on phosphate liberation. Magnesium salts enhanced phosphate liberation by preaged Mw both in the presence and absence of DNP. Calcium was virtually without effect in preaged Mw. </br></br>Oxalacetate enhanced phosphate liberation from ATP by fresh Mw. This dicarboxylic acid as well as succinate and L-malate depressed the </br>effect of DNP on phosphate liberation. Fatty acids also depressed the </br>effect of DNP. Caprylate enhanced phosphate liberation, probably be- </br>cause of its surface activity. </br></br>The thiol inhibitor, p-chloromercuribenzoate, strongly depressed the effect of DNP; iodoacetate and o-iodosobenzoate did not.</br></br>''Continued in Free Text''ate did not. ''Continued in Free Text'')
  • Freitas-Correa 2013 Stem Cell Res  + (2,4-Dinitrophenol (DNP) is a neuroprotecti2,4-Dinitrophenol (DNP) is a neuroprotective compound previously shown to promote neuronal differentiation in a neuroblastoma cell line and neurite outgrowth in primary neurons. Here, we tested the hypothesis that DNP could induce neurogenesis in embryonic stem cells (ESCs). Murine ESCs, grown as embryoid bodies (EBs), were exposed to 20μM DNP (or vehicle) for 4days. Significant increases in the proportion of nestin- and β-tubulin III-positive cells were detected after EB exposure to DNP, accompanied by enhanced glial fibrillary acidic protein (GFAP), phosphorylated extracellular signal-regulated kinase (p-ERK) and ATP-linked oxygen consumption, thought to mediate DNP-induced neural differentiation. DNP further protected ESCs from cell death, as indicated by reduced caspase-3 positive cells, and increased proliferation. Cell migration from EBs was significantly higher in DNP-treated EBs, and migrating cells were positive for nestin, ß-tubulin III and MAP2, similar to that observed with retinoic acid (RA)-treated EBs. Compared to RA, however, DNP exerted a marked neuritogenic effect on differentiating ESCs, increasing the average length and number of neurites per cell. Results establish that DNP induces neural differentiation of ESCs, accompanied by cell proliferation, migration and neuritogenesis, suggesting that DNP may be a novel tool to induce neurogenesis in embryonic stem cells.duce neurogenesis in embryonic stem cells.)
  • Sebollela 2010 Neurotox Res  + (2,4-Dinitrophenol (DNP) is classically kno2,4-Dinitrophenol (DNP) is classically known as a mitochondrial uncoupler and, at high concentrations, is toxic to a variety of cells. However, it has recently been shown that, at subtoxic concentrations, DNP protects neurons against a variety of insults and promotes neuronal differentiation and neuritogenesis. The molecular and cellular mechanisms underlying the beneficial neuroactive properties of DNP are still largely unknown. We have now used DNA microarray analysis to investigate changes in gene expression in rat hippocampal neurons in culture treated with low micromolar concentrations of DNP. Under conditions that did not affect neuronal viability, high-energy phosphate levels or mitochondrial oxygen consumption, DNP induced up-regulation of 275 genes and down-regulation of 231 genes. Significantly, several up-regulated genes were linked to intracellular cAMP signaling, known to be involved in neurite outgrowth, synaptic plasticity, and neuronal survival. Differential expression of specific genes was validated by quantitative RT-PCR using independent samples. Results shed light on molecular mechanisms underlying neuroprotection by DNP and point to possible targets for development of novel therapeutics for neurodegenerative disorders.rapeutics for neurodegenerative disorders.)
  • 2014 Mitochondrial Disease Clinical Conference  + (2014 Mitochondrial Disease Clinical Conference, Los Angeles, Ca US; [http://www.mitoaction.org/laconference 2014 Mitochondrial Disease Clinical Conference])
  • 2015 Spring PaduaMuscleDays  + (2015 Spring PaduaMuscleDays: Translational Myology in Aging and Neuromuscular Disorders, Padova, IT; [http://www.pagepressjournals.org/index.php/bam/announcement/view/176 2015 Spring PaduaMuscleDays].)
  • 2016 Spring PaduaMuscleDays Padua IT  + (2016 Spring PaduaMuscleDays: Muscle Decline in Aging and Neuromuscular Disorders - Mechanisms and Countermeasures, Padua, IT)
  • JSBBA 2017 Kyoto JP  + (2017 Annual Meeting of the Japan Society for Bioscience, Biotechnology, and Agrochemistry (JSBBA), Kyoto, Japan)
  • Movement and Cognition 2018 MA US  + (2018 world conference on Movement and Cognition, Boston, Massachusetts, USA, 2018)
  • Movement and Cognition 2019 Tel-Aviv IL  + (2019 World conference on Movement and Cognition, Tel-Aviv, Israel, 2019)
  • 2020 PaduaMuscleDays Padua IT  + (2020 PaduaMuscleDays - 30 years of translational research, Vitual Event, 2020)
  • Movement and Cognition 2020 Paris FR  + (2020 World conference on Movement and Cognition, Paris, France, 2020)
  • EBEC2018 Budapest HU  + (20<sup>th</sup> European Bioenergetics Conference 2018, Budapest, Hungary, 2018)
  • SHVM 2023 Graz AT  + (20th Annual Meeting of the Society for Heart and Vascular Metabolism (SHVM), Graz, Austria, 2023)
  • SFRR 2021 Virtual  + (20th Biennial Meeting of SFRR International, Virtual, 2021)
  • International Botanical Congress 2024 Madrid ES  + (20th International Botanical Congress (IBC), Madrid, ES, 2024)
  • EBEC2022 Aix-en-Provence FR  + (21<sup>st</sup> European Bioenergetics Conference 2022, Aix-en-Provence, France, 2022.)
  • EBEC2024 Innsbruck AT  + (22<sup>st</sup> European Bioenergetics Conference 2024, Innsbruck, Austria, 2024)
  • GFB 2023 Bedoin FR  + (22nd GFB conference, Bedoin, France, 2023)
  • 24th Kalorimetrietage 2021 Braunschweig DE  + (24th Kalorimetrietage, Braunschweig, Germany, 2021.)
  • 25th Krakow Conference on Endothelium 2017 PL  + (25<sup>th</sup> Krakow Conference on Endothelium, Krakow, Poland.)
  • SFRR 2018 Auckland NZ  + (26th Meeting for the Society for Free Radical Research Australasia SFRR(A), Auckland, New Zeland, 2018)
  • ECSS 2023 Paris FR  + (28<sup>th</sup> ECSS Congress, Paris, France, 2023)
  • 28th Congress of the Polish Physiological Society 2021 Virtual  + (28th Congress of the Polish Physiological Society, Virtual, 2021)
  • FEBS 2022 Mutters AT  + (2<sup>nd</sup> FEBS Workshop on Ageing and Regeneration, Mutters, Austria, 2022)
  • Cardiovascular Metabolic Disease 2015  + (2nd Annual Conference of the Prevention and Control of Cardiovascular Metabolic Disease, Wuhan, CN; post-conference workshop '''[[MiPNet20.11_IOC102_Wuhan | 102nd Oroboros O2k-Workshop]]'''.)
  • Mitochondria-Targeted Drug Development 2022 Boston US  + (2nd Annual Mitochondria-Targeted Drug Development, Boston MA, US, 2022.)
  • 2nd International Munich ROS Meeting 2018 Munich DE  + (2nd International Munich ROS Meeting, Munich, Germany, 2018)
  • 2nd Mitochondria Conference 2023 Lisbon PT  + (2nd Mitochondria Conference, Lisbon, Portugal, 2023.)
  • Pereira 2009 Biochem J  + (3-BrPA (3-bromopyruvate) is an alkylating 3-BrPA (3-bromopyruvate) is an alkylating agent with antitumoral activity on hepatocellular carcinoma. This compound inhibits cellular ATP production owing to its action on glycolysis and oxidative phosphorylation; however, the specific metabolic steps and mechanisms of 3-BrPA action in human hepatocellular</br>carcinomas, particularly its effects on mitochondrial energetics, are poorly understood. In the present study it was found that incubation of HepG2 cells with a low concentration of 3-BrPA for a short period (150 μMfor 30 min) significantly affected both glycolysis and mitochondrial respiratory functions. The activity of mitochondrial hexokinase was not inhibited by 150 μM 3-BrPA, but this concentration caused more than 70% inhibition of GAPDH (glyceraldehyde-3-phosphate dehydrogenase) and 3-phosphoglycerate kinase activities. Additionally, 3-BrPA treatment significantly impaired lactate production by HepG2 cells, even when glucose was withdrawn from the incubation medium.</br>Oxygen consumption of HepG2 cells supported by either pyruvate/malate or succinate was inhibited when cells were preincubated with 3-BrPA in glucose-free medium. On the other hand, when cells were pre-incubated in glucose-supplemented medium, oxygen consumption was affected only when succinate</br>was used as the oxidizable substrate. An increase in oligomycinindependent</br>respiration was observed in HepG2 cells treated with 3-BrPA only when incubated in glucose-supplemented medium, indicating that 3-BrPA induces mitochondrial proton leakage as well as blocking the electron transport system. The activity</br>of succinate dehydrogenase was inhibited by 70% by 3-BrPA treatment. These results suggest that the combined action of 3- BrPA on succinate dehydrogenase and on glycolysis, inhibiting steps downstream of the phosphorylation of glucose, play an important role in HepG2 cell death.lay an important role in HepG2 cell death.)