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• Movement and Cognition 2020 Paris FR  + (2020 World conference on Movement and Cognition, Paris, France, 2020)
• EBEC2018 Budapest HU  + (20^th 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^st European Bioenergetics Conference 2022, Aix-en-Provence, France, 2022.)
• EBEC2024 Innsbruck AT  + (22^st 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^th 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^th 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^nd 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.)
• 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.</br></br>The effect of 3BrPA was characterized in mice liver and kidney mitochondria, as well as in human HepG2 cells.</br></br>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.</br></br>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.</br></br>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  + (32^th 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  + (3^rd MiP''summer school'' on Mitochondrial Respiratory Physiology, 2009 June 17-23, Baton Rouge, Louisiana US.)
• Eugeny I. Schwartz Conference 2015  + (3^rd 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. </br>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).</br> </br>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).</br></br> </br>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  + (43^rd Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT))
• AICBC 2024 Navi Mumbai IN  + (46^th 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  + (4^th Annual Conference of the Society for Mitochondrial Research and Medicine, Kolkata, India.)
• MiPschool Druskininkai LT 2010  + (4^th MiP''summer school'' on Mitochondrial Respiratory Physiology, 2010 June 10-16, Druskininkai, Lithuania.)
• TrMAD2014  + (4^th 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 </br></br></br>== Program ==</br>:::: [https://www.metabolism-cancer.com/program/ here]</br></br>== Organizers ==</br>:::: The list of organizers can be found [https://www.metabolism-cancer.com/under-construction/ here]</br></br>== Registration ==</br>:::: [https://www.metabolism-cancer.com/registration/ Registration and more information]</br></br>== Oroboros at MetaboCancer 2021==</br>:::: [[Gnaiger Erich]]: Oroboros Instruments innovations - NextGen-O2k and Bioenergetics Communications, ''May 28th at 11:25''</br></br>=== Booth ===</br>:::: The Oroboros team is looking forward to welcome you at our Oroboros booth which will be available at this conference.</br></br></br>== Support ==</br>[[File:Template NextGen-O2k.jpg|right|350px|link=NextGen-O2k]]</br></br>[[Category:NextGen-O2k]]</br>:::: 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.</br><br/></br><br/></br><br/></br><br/> agreement No. 859770. <br/> <br/> <br/> <br/>)
• 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.</br></br>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.)
• Hanley 2005 J Physiol  + (5-Hydroxydecanoate (5-HD) blocks pharmacol … 5-Hydroxydecanoate (5-HD) blocks pharmacological and ischaemic preconditioning, and has been postulated to be a specific inhibitor of mitochondrial ATP-sensitive K+ (KATP) channels. However, recent work has shown that 5-HD is activated to 5-hydroxydecanoyl-CoA (5-HD-CoA), which is a substrate for the first step of β-oxidation. We have now analysed the complete β-oxidation of 5-HD-CoA using specially synthesised (and purified) substrates and enzymes, as well as isolated rat liver and heart mitochondria, and compared it with the metabolism of the physiological substrate decanoyl-CoA. At the second step of β-oxidation, catalysed by enoyl-CoA hydratase, enzyme kinetics were similar using either decenoyl-CoA or 5-hydroxydecenoyl-CoA as substrate. The last two steps were investigated using l-3-hydroxyacyl-CoA dehydrogenase (HAD) coupled to 3-ketoacyl-CoA thiolase. ''V''max for the metabolite of 5-HD (3,5-dihydroxydecanoyl-CoA) was fivefold slower than for the corresponding metabolite of decanoate (l-3-hydroxydecanoyl-CoA). The slower kinetics were not due to accumulation of d-3-hydroxyoctanoyl-CoA since this enantiomer did not inhibit HAD. Molecular modelling of HAD complexed with 3,5-dihydroxydecanoyl-CoA suggested that the 5-hydroxyl group could decrease HAD turnover rate by interacting with critical side chains. Consistent with the kinetic data, 5-hydroxydecanoyl-CoA alone acted as a weak substrate in isolated mitochondria, whereas addition of 100 μm 5-HD-CoA inhibited the metabolism of decanoyl-CoA or lauryl-carnitine. In conclusion, 5-HD is activated, transported into mitochondria and metabolised via β-oxidation, albeit with rate-limiting kinetics at the penultimate step. This creates a bottleneck for β-oxidation of fatty acids. The complex metabolic effects of 5-HD invalidate the use of 5-HD as a blocker of mitochondrial KATP channels in studies of preconditioning.TP channels in studies of preconditioning.)
• Mitchell 2011 Biochim Biophys Acta  + (50 years ago Peter Mitchell proposed the c … 50 years ago Peter Mitchell proposed the chemiosmotic hypothesis for which he was awarded the Nobel Prize for Chemistry in 1978. His comprehensive review on chemiosmotic coupling known as the first “Grey Book”, has been reprinted here with permission, to offer an electronic record and easy access to this important contribution to the biochemical literature. This remarkable account of Peter Mitchell's ideas originally published in 1966 is a landmark and must-read publication for any scientist in the field of bioenergetics. As far as was possible, the wording and format of the original publication have been retained. Some changes were required for consistency with BBA formats though these do not affect scientific meaning. A scanned version of the original publication is also provided as a downloadable file in Supplementary Information. See also Editorial in this issue by Peter R. Rich. Original title: CHEMIOSMOTIC COUPLING IN OXIDATIVE AND PHOTOSYNTHETIC PHOSPHORYLATION, by Peter Mitchell, Glynn Research Laboratories, Bodmin, Cornwall, England.h Laboratories, Bodmin, Cornwall, England.)
• ESCI 2021 Virtual  + (55^th ESCI meeting, Virtual, 2021)
• ESCI 2022 Bari IT  + (56^th ESCI meeting, Bari, Italy, 2022)
• ESCI 2023 Prague CZ  + (57^th ESCI meeting, Prague, Czech Republic, 2023)
• Targeting Mitochondria World Congress 2014  + (5^th Targeting Mitochondria World Congress - [http://www.targeting-mitochondria.com/ Targeting Mitochondria], Berlin DE)
• 5th Academic Symposium of Metabolic Biology Branch of Chinese Biophysical Society 2022 Zunyi CN  + (5th Academic Symposium of Metabolic Biology Branch of Chinese Biophysical Society, Zunyi, China, 2022)