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Griffiths 1995 Biochem J + (1. The yield of mitochondria isolated from … 1. 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 wh … 1. 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.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.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.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.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.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 was … 10 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 + (10th Conference of the Asian Society of Mitochondrial Research and Medicine - [http://asmrm2013.com/common_files/mess.asp ASMRM 2013], Seoul KR)
MiP2014 + (10th 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 Mitochondri … 10th Translational Research in Mitochondria/Metabolism, Aging, and Disease (TRiMAD) Conference, Pennsylvania, United States, 2023 == General information ==:::: 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])== Venue == :::: University of Pittsburgh:::: Bridgeside Point 1, 5th Floor:::: 100 Technology Drive:::: Pittsburgh, PA 15219== Organizers ==:::: University of Pittsburgh:::: Aging Institute:::: Center for Metabolism & Mitochondrial Medicine== Program ==:::: Please find the programme [https://aging.pitt.edu/event/trimad-2023/ here]== Registration ==:::: [https://forms.office.com/pages/responsepage.aspx?id=ifT5nqDg606HzDpSYRL9DXg8U8hQ84RKssucFsBERrBURTU2T1lFR01DS0hYNlZGRjNDTzg2QVJRSC4u Register here] == Lecturers and tutors ==:::: 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 Mitochond … 10th World Congress on Targeting Mitochondria, Berlin, Germany, 2019 == General information == :::: Flyer available for [http://wiki.oroboros.at/images/7/7f/Berlin_2019.pdf download]== Venue == :::: INTERCONINENTAL BERLIN HOTEL:::: Budapester Str. 2, 10787:::: Berlin, Germany::::[https://targeting-mitochondria.com/venue Hotel and Travel]== Programme ==:::: [https://targeting-mitochondria.com/preliminary-program here]== Speakers == :::: List of speakers can be found [https://targeting-mitochondria.com/speakers-2019 here]== Registration ==:::: [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 Mitochond … 11th World Congress on Targeting Mitochondria, Virtual, 2020 == General information == :::: 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.== Programme ==:::: [https://targeting-mitochondria.com/preliminary-program here]== Speakers == :::: List of speakers can be found [https://targeting-mitochondria.com/speakers here]== Registration ==:::: [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 + (12th 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 a … 12th International Conference on Obesity and Eating Disorders, Vienna, Austria, 2023 == General Information == :::: The theme of the conference is "New Emerging Challenges in Obesity and their Prevention"== Venue ==:::: [https://obesity.euroscicon.com/ How to get there]== Program ==:::: Program available [https://obesity.euroscicon.com/program-schedule here]== Organizers ==:::: The list of organizers can be found [https://obesity.euroscicon.com/organizing-committee here]== Registration ==:::: [https://obesity.euroscicon.com/registration Registration and more information]:::: Early registration deadline: 203-01-27:::: 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 == Venue == ::::[https://ipc2021.com/logistic-information/ Venue and how to get there]== Programme ==:::: [https://ipc2021.com/scientific-program/ here]== Speakers == :::: List of speakers can be found [https://ipc2021.com/invited-speakers/ here]== Organizers ==:::: The list of organizers can be found [https://ipc2021.com/local-organizing-committee-scientific-committee/ here]== Registration ==:::: [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, Aus … 13th Life Sciences Meeting, Innsbruck, Austria, 2018 __TOC__== General information== :::: 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“. == Venue == :::: Center for Chemistry and Biomedicine (CCB):::: Innrain 80, 6020 Innsbruck:::: [http://biocenter.i-med.ac.at/ Location]== Organizers ==:::: Medical University of Innsbruck==Oroboros presentation ==:::: 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]]:::: POSTER: Marie Skłodowska-Curie Project '''[[TRACT]]''' [[Chang Shao-Chiang]]: [[Chang 2018 Life Sciences Meeting 2018 Innsbruck AT|pH dependence of mitochondrial respiration and H2O2 production in oral cancer cells – a pilot study.]]:::: 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)
13th ÖGMBT Annual Meeting 2021 Innsbruck AT + (13th ÖGMBT Annual Meeting, Virtual, 2021)
FAOBMB 2015 Hyderabad IN + (14th 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 + (17th 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 + (19th 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 == Venue == :::: Faculty of Natural Sciences (NAWI) of the Paris Lodron University Salzburg (PLUS):::: Venue address: Hellbrunnerstrasse 34, 5020 Salzburg, Austria.:::: [http://salzburg2021.photobiology.eu/congress-venue more information]== Program ==:::: [http://salzburg2021.photobiology.eu/ here]== Speakers == :::: List of speakers can be found [http://salzburg2021.photobiology.eu/ here]== Organizers ==:::: The list of organizers can be found [http://salzburg2021.photobiology.eu/organizing-committee here]== Registration ==:::: [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 + (1st 1st FEBS Workshop “Redox Medicine Workshop, Luso, Portugal, 2023)
MiPschool Schroecken AT 2007 + (1st 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 D3</s … 1α,25-Dihydroxyvitamin D3 (1,25-D3) 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-D3 on GGT on Sertoli cell functions from 30-day-old immature rat testis. Results demonstrated that 1,25-D3 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-D3 did not change reduced glutathione (GSH) amount or oxygen consumption, and diminished Sertoli cell death. These findings demonstrate that 1,25-D3 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 dihydrorhoda … 2',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. The microsomal and supernatant fractions did not exhibit this effect. 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. With both fresh and preaged Mw, the response to DNP was much greater 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. Oxalacetate enhanced phosphate liberation from ATP by fresh Mw. This dicarboxylic acid as well as succinate and L-malate depressed the effect of DNP on phosphate liberation. Fatty acids also depressed the effect of DNP. Caprylate enhanced phosphate liberation, probably be- cause of its surface activity. The thiol inhibitor, p-chloromercuribenzoate, strongly depressed the effect of DNP; iodoacetate and o-iodosobenzoate did not.''Continued in Free Text''ate did not. ''Continued in Free Text'')
Freitas-Correa 2013 Stem Cell Res + (2,4-Dinitrophenol (DNP) is a neuroprotecti … 2,4-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 kno … 2,4-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])

(2014 Mitochondrial Disease Clinical Conference, Los Angeles, Ca US; [htt)

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 + (20th 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 + (21st European Bioenergetics Conference 2022, Aix-en-Provence, France, 2022.)
EBEC2024 Innsbruck AT + (22st 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 + (25th 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 + (28th 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 + (2nd 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 hepatocellularcarcinomas, 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.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 succinatewas used as the oxidizable substrate. An increase in oligomycinindependentrespiration 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 activityof 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.)
Jardim-Messeder 2012 Int J Biochem Cell Biol + (3-Bromopyruvate (3BrPA) is an antitumor ag … 3-Bromopyruvate (3BrPA) is an antitumor agent that alkylates the thiol groups of enzymes and has been proposed as a treatment for neoplasias because of its specific reactivity with metabolic energy transducing enzymes in tumor cells. In this study, we show that the sarco/endoplasmic reticulum calcium (Ca2+) ATPase (SERCA) type 1 is one of the target enzymes of 3BrPA activity. Sarco/endoplasmic reticulum vesicles (SRV) were incubated in the presence of 1mM 3BrPA, which was unable to inhibit the ATPase activity of SERCA. However, Ca2+-uptake activity was significantly inhibited by 80% with 150μM 3BrPA. These results indicate that 3BrPA has the ability to uncouple the ATP hydrolysis from the calcium transport activities. In addition, we observed that the inclusion of 2mM reduced glutathione (GSH) in the reaction medium with different 3BrPA concentrations promoted an increase in 40% in ATPase activity and protects the inhibition promoted by 3BrPA in calcium uptake activity. This derivatization is accompanied by a decrease of reduced cysteine (Cys), suggesting that GSH and 3BrPA increases SERCA activity and transport by pyruvylation and/or S-glutathiolation mediated by GSH at a critical Cys residues of the SERCA.hiolation mediated by GSH at a critical Cys residues of the SERCA.)
Jardim-Messeder 2016 Anticancer Res + (3-bromopyruvate (3BrPA) is an antitumor ag … 3-bromopyruvate (3BrPA) is an antitumor agent able to inhibit aerobic glycolysis and oxidative phosphorylation, therefore inducing cell death. However, cancer cells are also highly dependent of glutaminolysis and tricarboxylic acid cycle (TCA) regarding survival and 3BrPA action in these metabolic routes is poorly understood.The effect of 3BrPA was characterized in mice liver and kidney mitochondria, as well as in human HepG2 cells.Low concentration of 3-BrPA significantly affected both glutaminolysis and TCA cycle functions, through inhibition of isocitrate dehydrogenase, α-ketoglutarate dehydrogenase and succinate dehydrogenase. Additionally, 3-BrPA treatment significantly decreased the reduced status of thiol groups in HepG2 cells without proportional increase of oxidizing groups, suggesting that these chemical groups are the target of alkylation reactions induced by 3-BrPA.This work demonstrates, for the first time, the effect of 3-BrPA in glutaminolysis and TCA cycle. Our results suggest that the combined action of 3-BrPA in glutaminolysis, TCA and glycolysis, inhibiting steps downstream of the glucose and glutamine metabolism, has an antitumor effect.Copyright© 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.John G. Delinassios), All rights reserved.)
Vevera 2016 Physiol Res + (3-hydroxy-3-methylglutaryl-coenzyme A (HMG … 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used drugs for lowering blood lipid levels and preventing cardiovascular diseases. However, statins can have serious adverse effects, which may be related to development of mitochondrial dysfunctions. The aim of study was to demonstrate the ''in vivo'' effect of high and therapeutic doses of statins on mitochondrial respiration in blood platelets. Model approach was used model in the study. Simvastatin was administered to rats at a high dose for 4 weeks. Humans were treated with therapeutic doses of rosuvastatin or atorvastatin for 6 weeks. Platelet mitochondrial respiration was measured using high-resolution respirometry. In rats, a significantly lower physiological respiratory rate was found in intact platelets of simvastatin-treated rats compared to controls. In humans, no significant changes in mitochondrial respiration were detected in intact platelets; however, decreased complex I-linked respiration was observed after statin treatment in permeabilized platelets. We propose that the small ''in vivo'' effect of statins on platelet energy metabolism can be attributed to drug effects on complex I of the electron transport system. Both intact and permeabilized platelets can be used as a readily available biological model to study changes in cellular energy metabolism in patients treated with statins.tabolism in patients treated with statins.)
JACBS Taipei TW + (32th Joint Annual Conference of Biomedical Science, Taipei, Taiwan.)
APS2020 Chicago US + (32nd APS Annual Convention, Chicago, USA, 2020)
36th Congress Czech Nutrition Society 2020 Hradec Kralove CZ + (36th annual international congress of Czech Nutrition Society, Hradec Kralove, Czech Republic, 2020)
37th Annual Meeting of the ISHR-ES 2023 Porto PT + (37th Annual Meeting of the ISHR-ES, Porto, Portugal, 2023)
MiPschool Baton Rouge LA US 2009 + (3rd MiP''summer school'' on Mitochondrial Respiratory Physiology, 2009 June 17-23, Baton Rouge, Louisiana US.)
Eugeny I. Schwartz Conference 2015 + (3rd Russian Congress with International Participation “Molecular Basis of Clinical Medicine: State-of-the-Art and Perspectives” dedicated to the memory of Eugeny I. Schwartz, St. Petersburg , Russia;)
Ophthalmology Conference 2018 Rome IT + (3rd Edition of International Conference on Eye and Vision, Rome, Italy; 2018)
METABO & Cancer 2019 Marseille FR + (3rd edition - Metabolism and Cancer Meeting, Marseille, France, 2019)
MacDonald 2014 Abstract MiP2014 + (4-hydroxy-2-oxoglutarate aldolase (HOGA) i … 4-hydroxy-2-oxoglutarate aldolase (HOGA) is a bi-functional mitochondrial enzyme, expressed predominantly in liver and kidney. HOGA is involved in the hydroxyproline degradation pathway (HOGglyoxylate+pyruvate), and mutations in HOGA result in primary Hyperoxaluria Type III, characterized by excessive oxalate production and kidney stone deposition [1]. We hypothesized that HOGA may also be involved in the TCA cycle as an oxaloacetate decarboxylase (oxaloacetatepyruvate; Fig. 1), which may allow the TCA cycle to turnover in the absence of pyruvate and/or excess oxaloacetate. The kinetics of HOGA with substrates HOG and oxaloacetate were investigated by measuring the ''K''’m and ''k''cat of recombinant human HOGA, using an LDH-coupled microplate assay. The role of HOGA in the TCA cycle was investigated using mitochondria, isolated from rat liver and kidney, where HOGA is highly expressed, and brain and heart, where expression is lower. ADP-stimulated malate respiration was measured relative to ADP-malate + pyruvate (M:PM), using oxygraphy (Oroboros Oxygraph-2k, note malate was used as oxaloacetate cannot cross the inner mitochondrial membrane). While HOGA was 75% less efficient at cleaving oxaloacetate than its other substrate, HOG (''K''’m/''k''cat), the ''K''’m for oxaloacetate was within range of that estimated for TCA intermediates (''K''’m,ox=129±8 µM, ''k''cat,ox=0.52±0.01 s-1; ''K''’m,HOG=55±5 µM, ''k''cat,HOG=1.01±0.03 s-1). Overall, HOGA appears to use the same catalytic mechanism to cleave both HOG and oxaloacetate substrates. Interestingly, the TCA cycle intermediate a-ketoglutarate was found to be a competitive inhibitor of HOGA oxaloacetate decarboxylase activity (''K''i=2.8 mM). Mitochondria from rat liver had the highest M:PM respiration relative to all other organs (0.46±0.05, ''P''<0.05). Though kidney had a higher M:PM respiration than heart (0.27±0.02 vs 0.15±0.02, ''P''<0.05 in kidney and heart, respectively), brain respired as well as kidney (0.33±0.04). In summary, HOGA cleaves oxaloacetate and HOG using the same catalytic mechanism but was less efficient with oxaloacetate. Liver and kidney have high HOGA expression, and mitochondria from both respire significantly better on malate relative to PM than heart mitochondria. The brain respires just as well with malate compared to kidney, and this may be due to high expression of malic enzyme, which can convert malate directly to pyruvate (Fig. 1). Malate supported respiration in HOGA overexpressing cells will confirm the direct role of HOGA in the TCA cycle.ession of malic enzyme, which can convert malate directly to pyruvate (Fig. 1). Malate supported respiration in HOGA overexpressing cells will confirm the direct role of HOGA in the TCA cycle.)
MBSJ 2018 Yokohama JP + (41st Annual Meeting of the Molecular Biology Society of Japan, Yokohama, Japan, 2018.)
The 42nd Annual Meeting of The Molecular Biology Society of Japan + (42nd Annual Meeting of The Molecular Biology Society of Japan, Kurume, 2018)
ISOTT 2015 + (43rd Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT))
AICBC 2024 Navi Mumbai IN + (46th All India Cell Biology Conference, Navi Mumbai, India, 2024)
46th ISOBM Congress 2019 Athens GR + (46th annual congres of the International Society of Oncology and Biomarkers, Athens, Greece, 2019)
ESCI 2015 + (49th Annual Scientific Meeting of the European Society for Clinical Investigation, Cluj-Napoca, Romania; [http://www.esci.eu.com/meetings/ ESCI 2015])
SMRM2014 Manipal IN + (4th Annual Conference of the Society for Mitochondrial Research and Medicine, Kolkata, India.)
MiPschool Druskininkai LT 2010 + (4th MiP''summer school'' on Mitochondrial Respiratory Physiology, 2010 June 10-16, Druskininkai, Lithuania.)
TrMAD2014 + (4th Regional Translational Research in Mitochondria, Aging, and Disease Symposium, Pittsburgh, PA, US. [http://www.upci.upmc.edu/trmad/ TrMAD2014])
4th Global Chinese Symposium & The 8th Symposium for Cross-straits on Free Radical Biology and Medicine 2018 Macao CN + (4th Global Chinese Symposium & The 8th Symposium for Cross-straits, Hong Kong and Macao on Free Radical Biology and Medicine, Macao, China, 2018)
4th edition Metabolism & Cancer 2021 Virtual + (4th edition Metabolism & Cancer, Virtu … 4th edition Metabolism & Cancer, Virtual, 2021 == Program ==:::: [https://www.metabolism-cancer.com/program/ here]== Organizers ==:::: The list of organizers can be found [https://www.metabolism-cancer.com/under-construction/ here]== Registration ==:::: [https://www.metabolism-cancer.com/registration/ Registration and more information]== Oroboros at MetaboCancer 2021==:::: [[Gnaiger Erich]]: Oroboros Instruments innovations - NextGen-O2k and Bioenergetics Communications, ''May 28th at 11:25''=== Booth ===:::: The Oroboros team is looking forward to welcome you at our Oroboros booth which will be available at this conference.== Support ==[[File:Template NextGen-O2k.jpg|right|350px|link=NextGen-O2k]][[Category:NextGen-O2k]]:::: Supported by project NextGen-O2k which has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No. 859770. agreement No. 859770. )
MacPherson 2016 Am J Physiol Cell Physiol + (5'-AMP-activated protein kinase (AMPK) is … 5'-AMP-activated protein kinase (AMPK) is activated as a consequence of lipolysis and has been shown to play a role in regulation of adipose tissue mitochondrial content. Conversely, the inhibition of lipolysis has been reported to potentiate the induction of protein kinase A (PKA)-targeted genes involved in the regulation of oxidative metabolism. The purpose of the current study was to address these apparent discrepancies and to more fully examine the relationship between lipolysis, AMPK, and the β-adrenergic-mediated regulation of gene expression. In 3T3-L1 adipocytes, the adipose tissue triglyceride lipase (ATGL) inhibitor ATGListatin attenuated the Thr(172) phosphorylation of AMPK by a β3-adrenergic agonist (CL 316,243) independent of changes in PKA signaling. Similarly, CL 316,243-induced increases in the Thr(172) phosphorylation of AMPK were reduced in adipose tissue from whole body ATGL-deficient mice. Despite reductions in the activation of AMPK, the induction of PKA-targeted genes was intact or, in some cases, increased. Similarly, markers of mitochondrial content and respiration were increased in adipose tissue from ATGL knockout mice independent of changes in the Thr(172) phosphorylation of AMPK. Taken together, our data provide evidence that AMPK is not required for the regulation of adipose tissue oxidative capacity in conditions of reduced fatty acid release.Copyright © 2016 the American Physiological Society.© 2016 the American Physiological Society.)
Stride 2012 Front Physiol + (5'-adenosine monophosphate-activated prote … 5'-adenosine monophosphate-activated protein kinase (AMPK) is considered central in regulation of energy status and substrate utilization within cells. In heart failure the energetic state is compromised and substrate metabolism is altered. We hypothesized that this could be linked to changes in AMPK activity and we therefore investigated mitochondrial oxidative phosphorylation capacity from the oxidation of long- and medium-chain fatty acids (LCFA and MCFA) in cardiomyocytes from young and old mice expressing a dominant negative AMPKα2 (AMPKα2-KD) construct and their wildtype (WT) littermates. We found a 35-45% (P < 0.05) lower mitochondrial capacity for oxidizing MCFA in AMPKα2-KD of both age-groups, compared to WT. This coincided with marked decreases in protein expression (19/29%, P < 0.05) and activity (14/21%, P < 0.05) of 3-hydroxyacyl-CoA-dehydrogenase (HAD), in young and old AMPKα2-KD mice, respectively, compared to WT. Maximal LCFA oxidation capacity was similar in AMPKα2-KD and WT mice independently of age implying that LCFA-transport into the mitochondria was unaffected by loss of AMPK activity or progressing age. Expression of regulatory proteins of glycolysis and glycogen breakdown showed equivocal effects of age and genotype. These results illustrate that AMPK is necessary for normal mitochondrial function in the heart and that decreased AMPK activity may lead to an altered energetic state as a consequence of reduced capacity to oxidize MCFA. We did not identify any clear aging effects on mitochondrial function. any clear aging effects on mitochondrial function.)