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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 Additionally, 3-BrPA treatment significantly impaired lactate production by HepG2 cells, even when glucose was withdrawn from the incubation medium.Oxygen consumption of HepG2 cells supported by either pyruvate/malate or succinate was inhibited when cells were preincubated with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.)
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 + (55th ESCI meeting, Virtual, 2021)
ESCI 2022 Bari IT + (56th ESCI meeting, Bari, Italy, 2022)
ESCI 2023 Prague CZ + (57th ESCI meeting, Prague, Czech Republic, 2023)
Targeting Mitochondria World Congress 2014 + (5th 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)
5th International Conference of Mitochondrial Medicine + (5th International Mitochondrial Medicine Conference Mitochondrial, Online, 2021)
NHLBI Mitochondrial Biology Symposium 2019 Bethesda US + (5th NHLBI Mitochondrial Biology Symposium, … 5th NHLBI Mitochondrial Biology Symposium, Bethesda, Maryland, USA, 2019 == General information == ::::On September 26-27, 2019, experts from around the world will gather on the NIH Campus in Bethesda, Maryland to review advances in our understanding of how mitochondrial structure, function, and interactions within the cell contribute to diseases and aging; and to highlight recent progress made with animal models and therapeutic interventions.== Venue == :::: William H. Natcher Conference Center – Building 45:::: National Institutes of Health:::: 45 Center Drive:::: Bethesda, MD 20814:::: [https://2019mbs.com/meeting-venue/ How to get there]== Organizer ==:::: [https://2019mbs.com/organizers/ Information available here]== Programme ==:::: [https://2019mbs.com/agenda/ Agenda]== Speakers == :::: List of speakers can be found [https://2019mbs.com/featured-speakers/ here]== Registration ==:::: [https://www.eventbrite.com/e/the-2019-nhlbi-mitochondrial-biology-symposium-registration-54765893261 Registration and more information]:::: The abstracts submission deadline is Friday, June 28, 2019, at 11:59PM EST. :::: All submissions must be made through the abstract submission portal. :::: Abstracts should be no longer than 500 words and include four clearly identifiable components: Background, Methods, Results, and Conclusion. :::: Abstracts will be reviewed by the Organizing Committee. Acceptance will be based on the quality of the abstract and availability of space. Four high-quality abstracts will be selected for oral presentation.ts will be selected for oral presentation.)
5th edition Metabolism & Cancer 2023 Nice FR + (5th edition Metabolism & Cancer, Nice, … 5th edition Metabolism & Cancer, Nice, France, 2023 == Venue ==:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 How to get there]== Program ==:::: Program available [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]== Organizers ==:::: The list of organizers can be found [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 here]== Registration ==:::: [https://www.metabolism-cancer.com/?utm_source=altemail&utm_medium=email&utm_campaign=2023-01-04%20METABO%202023%201 Registration and more information]utm_campaign=2023-01-04%20METABO%202023%201 Registration and more information])
BPS19 2019 Baltimore US + (63rd Annual Meeting of the Biophysical Soc … 63rd Annual Meeting of the Biophysical Society, Baltimore, Maryland USA, 2019 == General information==:::: The Biophysical Society meeting is the only major scientific meeting in the United States that routinely includes bioenergetics and mitochondrial topics. The Bioenergetics, Mitochondria, and Metabolism Subgroup has its two symposia on the first day of the meeting, March 2nd, and these two symposia have a distinguished group of speakers who are leaders in the field of bioenergetics. == Venue == :::: Baltimore Convention Center:::: 1 W. Pratt Street:::: Baltimore, Maryland 21201::::[https://www.biophysics.org/2019meeting/hotel-travel Hotel and Travel]== Programme ==:::: [https://www.biophysics.org/2019meeting/program here]== Registration ==:::: [https://www.biophysics.org/2019meeting/registration Registration and more information]tration Registration and more information])
AMI 2023 Jhansi IN + (64th Annual International Conference of the Associate of Microbiologists of India, Jhansi, India, 2023)
BPS2023 San Diego US + (67th Annual Meeting of the Biophysical Society, San Diego, California, USA, 2023)
ISOTT 2017 Halle/Saale DE + (6th 45th Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT), Halle/Saale, Germany.)
6th Annual Conference of Chinese Society for Neurobiological Control of Metabolism 2024 Quanzhou CN + (6th Annual Conference of Chinese Society for Neurobiological Control of Metabolism, Quanzhou, China, 2024)
SMRM2017 New Delhi IN + (6th Annual Conference of the Society for Mitochondrial Research and Medicine, New Delhi, India.)
MiPschool Copenhagen DK 2013 + (6th MiP''summer school'' on Mitochondrial Physiology, 2013 August 26-30, Copenhagen, Denmark.)
6th Biannual Meeting on Mitochondria Apoptosis & Cancer 2019 Prague CZ + (6th Biannual Meeting on Mitochondria Apoptosis & Cancer, Prague, Czech Republic, 2019)
6th EU-Cardioprotection Meeting 2021 Riga LV + (6th EU-Cardioprotection WG Meeting CA16625 on mito and metabolism as targets for cardioprotection., Virtual Event, 2021)
6th International Conference on Tumor Microenvironment and Cellular Stress 2019 Crete GR + (6th International Conference on Tumor Microenvironment and Cellular Stress: Signaling, Metabolism, Imaging and Therapeutic Targets, Chania, Crete, Greece, 2019)

6th Research Day Innsbruck AT + (6th Research Day, Innsbruck, Austria, 2023)

77th Annual Meeting of the JCA 2018 Osaka JP + (77th Annual Meeting of the Japanese Cancer Association at the Osaka International Convention Center and RIHGA, Osaka, Japan, 2018)
The 77th Japanese Society of Physical Fitness and Sports Medicine 2022 Tochigi JP + (77th Japanese Society of Physical Fitness and Sports Medicine, Tochigi, 2022)
ISOTT 2018 Seoul KR + (7th 46th Annual Meeting of the International Society on Oxygen Transport to Tissue (ISOTT). Seoul, South Korea, 2018)
ISAP 2021 Virtual + (7th Conference of the International Society for Applied Phycology - ISAP2021, Tsukuba, Japan, 2021)
7th European Phycological Congress 2019 Zagreb HR + (7th European Phycological Congress, Zagreb, Croatia, 2019)
7th Molecular Mechanisms of Axon Degeneration Meeting Loch Lomond GB + (7th Molecular Mechanisms of Axon Degeneration Meeting, Loch Lomond, Scotland, Great Britain, 2019)
7th World Congress on Targeting Microbiota 2019 Krakow PL + (7th World Congress on Targeting Microbiota … 7th World Congress on Targeting Microbiota, Krakow, Poland, 2019 == Venue == :::: Park Inn by Radisson Krakow Hotel:::: Ul. Monte Cassino 2 PL:::: 30337 - Krakow - Poland:::: [https://www.microbiota-site.com/venue.html More information]== Organizer ==:::: [https://www.microbiota-site.com/committee.html Information available here]== Programme ==:::: [https://www.microbiota-site.com/images/2019/PDF/Targeting_Microbiota_2019_Agenda_-_V7.pdf Agenda]== Speakers == :::: List of speakers can be found [https://www.microbiota-site.com/microbiota-2019-speakers.html here]== Registration ==:::: [https://www.microbiota-site.com/registrations.html Registration and more information]ns.html Registration and more information])
MiPschool London 2015 + (8th MiP''school'' on Mitochondrial Physiology, 2015 Apr 20-24, London, UK.)
SMRM2020 Virtual + (8th Annual Meeting of the Society for Mitochondria Research and Medicine-India , Virtual.)
8th SMRM and Mitochondria-Metabolism Network Meeting 2020 Pune IN + (8th SMRM and Mitochondria-Metabolism Netwo … 8th SMRM and Mitochondria-Metabolism Network Meeting, Pune, India, 2020 == General information == :::: Flyer available for [https://www.mitoeagle.org/images/b/b2/8th_SMRM_and_Mitochondria-Metabolism_Network_Meeting_Poster.pdf download]== Venue == :::: Indian Institute of Science Education and Research (ISER Pune):::: Dr. Homi Bhabha Road:::: Pashan, Pune 411 008:::: INDIA::::[http://www.iiserpune.ac.in/facilities/guesthouse-cum-convention-centre Hotel and Travel]== Programme ==:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=12&confId=7288 here]== Speakers == :::: List of speakers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=0&confId=7288 here]== Organizers ==:::: The list of organizers can be found [https://indico.tifr.res.in/indico/internalPage.py?pageId=9&confId=7288 here]== Registration ==:::: [https://indico.tifr.res.in/indico/internalPage.py?pageId=6&confId=7288 Registration and more information]ageId=6&confId=7288 Registration and more information])
TriMAD Sysposium 2018 Pennsylvania US + (8th Translational Research in Mitochondria … 8th Translational Research in Mitochondria, Aging, and Disease (TRiMAD) Symposium, Pennsylvania, United States, 2018 == 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 == :::: The Pennsylvania State University:::: 100 Huck Life Sciences Building:::: University Park, Pennsylvania 16802:::: [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/directions-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx directions]== Organizers ==:::: Kateryna Makova, PhD - Penn State, University Park:::: Donna Korzick, PhD - Penn State, University Park[[File:Image001.jpg|right|550px]]== Programme ==:::: Please find the programme [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/agenda-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx here]== Registration ==:::: [https://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/registration-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx?fqp=true Register here] == Lecturers and tutors ==:::: The list of speakers can be found [http://www.cvent.com/events/8th-regional-translational-research-in-mitochondria-aging-and-disease-symposium/custom-18-16730cf0fe2c47a1b79f1a3b9ab0b364.aspx here]6730cf0fe2c47a1b79f1a3b9ab0b364.aspx here])
SBC 2023 Goa IN + (92nd Annual Meet of The Society of Biological Chemists, Goa, India, 2023)
Annual Meeting of the DPG 2016 Luebeck DE + (95th Annual Meeting of the DPG, [http://www.dpg2016.de/ DPG 2016], Luebeck, DE)
ASMRM 2012 Bejing CN + (9th Conference of t … 9th Conference of the Asian Society of Mitochondrial Research and Medicine and 5th Conference of Chinese Society of Mitochondrial Research and Medicine (Chinese-Mit), [http://asmrm2012.csp.escience.cn/dct/page/65540 ASMRM 2012], Bejing CN://asmrm2012.csp.escience.cn/dct/page/65540 ASMRM 2012], Bejing CN)
DNA Forensics 2014 + (9th International Y-chromosome workshop & 6th International EMPOP meeting, Brussels, Belgium; DNA Forensics 2014)
MiPschool Greenville 2015 + (9th MiP''school'' f … 9th MiP''school'' for cellular bioenergetics and mitochondrial physiology students, 2015 Aug 10-14, Greenville, US.» [http://www.ecu.edu/cs-admin/news/mip.cfm '''Global conference highlights mitochondria expertise at ECU'''], by Kathryn Kennedy ECU News Services.tise at ECU'''], by Kathryn Kennedy ECU News Services.)
SMRM2023 Hyderabad IN + (9th Annual Conference of the SMRM, Hyderabad, India.)
9th ÖGMBT Annual Meeting & 8th Life Science Meeting 2017 Innsbruck AT + (9th ÖGMBT Annual Meeting & 8th Life Science Meeting, Innsbruck, Austria)
Crispim 2019 MitoFit Preprint Arch EA + ( ::: Version 2 ('''v2''') '' … ::: Version 2 ('''v2''') '''2019-06-27''' [https://www.mitofit.org/images/6/68/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.v2.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007.v2]; v1 2019-06-17 [https://wiki.oroboros.at/images/8/81/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007]::: Version 1 (v1) [https://wiki.oroboros.at/images/8/81/Crispim_2019_MitoFit_Preprint_Arch_doi_10.26124mitofitea19.MiPSchool.0007.pdf doi:10.26124/mitofit:ea19.MiPSchool.0007]== Although atovaquone is one of the newest antimalarial compounds discovered, resistant parasites have already been reported1. Atovaquone mechanism of action is established to be the competition with ubiquinol (UQH2) for the bc1 union at mitochondrial cytochrome bc1 complex and preventing the parasite from maintaining an oxidized ubiquinone (UQ) pool, essential for the DHODH activity and consequently for the pyrimidine's biosynthesis. In this sense, possible inhibitors of the ubiquinone biosynthesis pathway would be candidates by stimulating the effects of atovaquone. 4-nitrobenzoate (4-NB) is a well-known inhibitor of 4HPT (4-hydroxybenzoate polyprenyltransferase), the first enzyme of UQ biosynthesis. 4-NB also showed an important effect on reducing the UQs pool in P. falciparum. Herein is presenting the effect of atovaquone and 4-NB on parasitic respiration UQ biosynthesis. The purpose of this study was to better understand the atovaquone mechanism of action in a molecular scale, drug target potential of UQ biosynthesis. Oxygen consumption assays revealed 4-NB potentiates atovaquone mitochondrial effects and showed itself the ability to decrease the respiration rate. ==- ''Extended abstract''crease the respiration rate. == - ''Extended abstract'' )
Gnaiger 2019 MitoFit Preprints Editorial + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2019-04-24''' [http://www.mitofit.org/images/d/d3/Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf doi:10.26124/mitofit:190002.v2]::: Version 1 (v1) 2019-04-01 [http://www.mitofit.org/images/archive/d/d3/20190424180311%21Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf doi:10.26124/mitofit:190002] - [http://www.mitofit.org/index.php/File:Gnaiger_2019_MitoFit_Preprint_Arch_doi_10.26124_mitofit_190002.v2.pdf#Links_to_all_versions »Link to all versions«]A manuscript in preparation for publication on ‘Mitochondrial states and rates’ is the first preprint posted on ''[[MitoFit Preprints]]'' (Gnaiger ''et al'' 2019). It actually triggered the initiation of a preprint server for mitochondrial physiology and bioenergetics. This editorial presents the story behind starting ''MitoFit Preprints'', to develop a vision of science communication beyond traditional journal and preprint publication. This is an open invitation to scientists of mitochondrial physiology and bioenergetics to join the preprint community by submitting manuscripts as preprints. We face the ''reproducibility crisis'' in the battle to separate doubtful data from relevant information. This is linked to the ''inflation crisis'' emanating from an exponential increase of scientific articles published per day. Unsustainable exponential growth leads to the ''value-impact crisis'' in the struggle to forge scientific innovation into knowledge and community benefits. forge scientific innovation into knowledge and community benefits. )
Gnaiger 2020 MitoFit x + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2021-09-06''' [https://www.mitofit.org/images/4/4a/Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf doi:10.26124/mitofit:200004.v2]::: Version 1 ('''v1''') 2020-08-11 [https://wiki.oroboros.at/images/archive/4/4a/20210906072525%21Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf doi:10.26124/mitofit:200004] — [https://www.mitofit.org/index.php/File:Gnaiger_MitoFit_Preprint_Arch_2020.4_doi_10.26214mitofit.200004.pdf »Link to all versions«]“The International System of Units, the SI, has been used around the world as the preferred system of units, the basic language for science, technology, industry and trade since it was established in 1960.” This statement heralds the 9th edition of the SI released on 2019-May-20. An new approach was introduced by defining the SI base units ― and thus the abstract SI units in general ― by their relation to fixed numerical values of fundamental constants of nature. Previous definitions of abstract units relied on a reference to concrete individual things realized as material artefacts, such as the International Prototype of the Kilogram (IPK). The (general) abstract unit ‘kilogram’ had to be calibrated in balance against an (individual) ‘entetic’ unit defining “1 kg” as a reference for the unit of mass and the mole [mol] as the unit of amount. Now the SI defines the mole as the fixed number of entities given by the Avogadro constant ''N''A. The elementary charge ''e'' is a fixed number of charges per proton. Amount and charge are thus in a fixed relation to the count of elementary entities ''U''''X'' [x]. Count, amount, and charge are isomorphic elementary quantities. Amount and charge are linked to the count ''N''''X'' = ''N''∙''U''''X'' with elementary unit x by fixed conversion constants ''N''A-1 [mol∙x−1] and ''e'' [C∙x−1], respectively. The SI does not use the elementary unit x. This causes a number of formal inconsistencies as discussed in the present communication on Euclid’s unit, which is ''U''''X'', and Euclid’s number, which is a count ''N''''X''.sistencies as discussed in the present communication on Euclid’s unit, which is ''U''''X'', and Euclid’s number, which is a count ''N''''X''. )
Baglivo 2022 MitoFit-QC + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2022-05-09''' [https://wiki.oroboros.at/images/c/c8/Baglivo_2022_MitoFit-QC.pdf doi:10.26124/mitofit:2022-0018.v2]::: Version 1 (v1) 2022-05-05 [https://wiki.oroboros.at/images/archive/c/c8/20220506062726%21Baglivo_2022_MitoFit-QC.pdf doi:10.26124/mitofit:2022-0018.v1] - [https://wiki.oroboros.at/index.php/File:Baglivo_2022_MitoFit-QC.pdf »Link to all versions«][[File:Baglivo 2022 MitoFit QC graphical-abstract.png|right|300px|Graphical abstract]][[Baglivo 2022 Abstract Bioblast]]: Evaluation of instrumental reproducibility is a primary component of quality control to quantify the precision and limit of detection of analytical procedures. A pre-analytical instrumental standard operating procedure (SOP) is implemented in high-resolution respirometry consisting of: (''1'') a daily SOP-POS for air calibration of the polarographic oxygen sensor (POS) in terms of oxygen concentration ''c''O2 [µM]. This is part of the ''sensor test'' to evaluate POS performance; (''2'') a monthly SOP-BG starting with the SOP-POS followed by the ''chamber test'' quantifying the instrumental O2 background. The chamber test focuses on the slope d''c''O2/d''t'' [pmol∙s−1∙mL−1] to determine O2 consumption by the POS and O2 backdiffusion into the chamber as a function of ''c''O2 in the absence of sample. Finally, zero O2 calibration completes the sensor test. We applied this SOP in a 3-year study using 48 Oroboros O2k chambers. Stability of air and zero O2 calibration signals was monitored throughout intervals of up to 8 months without sensor service. Maximum drift over 1 to 3 days was 0.06 pmol∙s−1∙mL−1, without persistence over time since drift was <0.004 pmol∙s−1∙mL−1 for time intervals of one month, corresponding to a drift per day of 0.2 % of the signal at air saturation. Instrumental O2 background -d''c''O2/d''t'' was stable within ±1 pmol∙s−1∙mL−1 when measured at monthly intervals. These results confirm the instrumental limit of detection of volume-specific O2 flux at ±1 pmol∙s−1∙mL−1. The instrumental SOP applied in the present study contributes to the generally applicable internal quality control management ensuring the unique reproducibility in high-resolution respirometry. These results confirm the instrumental limit of detection of volume-specific O2 flux at ±1 pmol∙s−1∙mL−1. The instrumental SOP applied in the present study contributes to the generally applicable internal quality control management ensuring the unique reproducibility in high-resolution respirometry. )
Gainutdinov 2022 MitoFit + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2022-08-16''' [https://wiki.oroboros.at/images/5/5a/Gainutdinov_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0015.v2]::: Version 1 (v1) 2022-04-21 [https://wiki.oroboros.at/images/archive/5/5a/20220816100352%21Gainutdinov_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0015]- [https://wiki.oroboros.at/index.php/File:Gainutdinov_2022_MitoFit.pdf »Link to all versions«]Amyotrophic lateral sclerosis (ALS) is a progressive, devastating, neurodegenerative disorder affecting upper and lower motor neurons. Common mechanisms of ALS pathogenesis are believed to be the disturbance of calcium homeostasis in the cell and dysfunction of mitochondria. Both factors mutually influence each other. As a result, chronic mitochondrial energy stress impairs fine cellular signaling and transport processes, leading to degeneration of motor neurons. In the current study we comparatively evaluated the cytosolic Ca2+ in healthy and ALS fibroblasts. We found that the mitochondrial calcium capacity in fibroblasts obtained from patients with sporadic (sALS) and familial (fALS) ALS differs between two subtypes and from that in healthy individuals. The changes of [Ca2+]cyt dynamics in ALS fibroblasts could be almost completely rescued by treatment with antioxidants (Trolox and CoQ10). These data confirm an important role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS.portant role of oxidative stress as a causative factor of mitochondrial dysfunction in ALS. )
Alencar 2022 MitoFit + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2022-07-07''' [https://wiki.oroboros.at/images/5/54/Alencar_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0009.v2]::: Version 1 (v1) 2022-04-07 [https://wiki.oroboros.at/images/archive/5/54/20220707123437%21Alencar_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0009.v1] - [https://wiki.oroboros.at/index.php/File:Alencar_2022_MitoFit.pdf »Link to all versions«][[Oliveira 2022 Abstract Bioblast]]: The parasite ''Trypanosoma brucei'' is the causative agent of sleeping sickness and involves an insect vector and a mammalian host through its complex life-cycle. ''T. brucei'' mammalian bloodstream forms (BSF) exhibit unique metabolic features including: ''i)'' reduced expression and activity of mitochondrial enzymes; ''ii)'' respiration mediated by the glycerol phosphate shuttle (GPSh) and the ''Trypanosome'' alternative oxidase (TAO) that is intrinsically uncoupled from generation of mitochondrial membrane potential; ''iii)'' maintenance of mitochondrial membrane potential by ATP hydrolysis through the reversal of F1Fo ATP synthase activity; ''iv)'' strong reliance on glycolysis to meet their energy demands; ''v)'' high susceptibility to oxidants. Here, we critically review the main metabolic features of BSF and provide a hypothesis to explain the unusual metabolic network and its biological significance for this parasite form. We postulate that intrinsically uncoupled respiration provided by GPSh-TAO system would act as a preventive antioxidant defense by limiting mitochondrial superoxide production and complementing the NADPH-dependent scavenging antioxidant defenses to maintain parasite redox balance. Given the uncoupled nature of the GPSh-TAO system, BSF would avoid programmed cell death processes by maintaining mitochondrial membrane potential through the reversal of ATP synthase activity using the ATP generated by glycolysis. This unique “metabolic design” in BSF has no biological parallel outside of Trypanosomatids and highlights the enormous diversity of the parasite mitochondrial processes to adapt to distinct environments.parasite mitochondrial processes to adapt to distinct environments. )
Ganguly 2022 MitoFit + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2022-11-10''' [https://wiki.oroboros.at/images/6/64/Ganguly_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0013.v2]::: Version 1 (v1) 2022-04-19 [https://wiki.oroboros.at/images/archive/6/64/20221110103433%21Ganguly_2022_MitoFit.pdf https://doi.org/10.26124/mitofit:2022-0013]- [https://wiki.oroboros.at/index.php/File:Ganguly_2022_MitoFit.pdf »Link to all versions«]Ferroptosis has been identified as a type of regulated cell death triggered by a diverse set of agents with implications in various diseases like cancer and neurodegenerative diseases. Ferroptosis is iron-dependent and accompanied by an accumulation of reactive oxygen species (ROS) and lipid oxidation products, a depletion of reduced glutathione, mitochondrial morphological alterations and the rupture of cell membrane; the process is inhibited by specific antioxidants like ferrostatin-1 and liproxstatin-1 and by other general antioxidants like the iron-chelator deferoxamine, vitamin E and N-acetylcysteine. However, the mechanism of cell death in ferroptosis subsequent to the accumulation of ROS and lipid oxidation products is not clearly established. We show here that the classical mitochondrial Complex I inhibitor rotenone (0.5 µM) causes death of SH-SY5Y cells (a human neuroblastoma cell line) over a period of 48 h accompanied by mitochondrial membrane depolarization and intracellular ATP depletion. This is associated with an intracellular accumulation of ROS and the lipid oxidation product malondialdehyde or MDA and a decrease in reduced glutathione content. All these processes are inhibited very conspicuously by specific inhibitors of ferroptosis such as ferrostatin-1 and liproxstatin-1. However, the decrease in Complex I activity upon rotenone-treatment of SH-SY5Y cells is not significantly recovered by ferrostatin-1 and liproxstatin-1. When the rotenone-treated cells are analyzed morphologically by Hoechst 33258 and propidium iodide (PI) staining, a mixed picture is noticed with densely fluorescent and condensed nuclei indicating apoptotic death of cells (Hoechst 33258) and also significant numbers of necrotic cells with bright red nuclei (PI staining).ant numbers of necrotic cells with bright red nuclei (PI staining). )
Roach 2022 MitoFit + ( ::: Version 2 ('''v2''') ''' … ::: Version 2 ('''v2''') '''2022-07-19''' [https://wiki.oroboros.at/images/d/d6/Roach_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0023.v2]::: Version 1 (v1) 2022-06-03 [https://wiki.oroboros.at/images/archive/d/d6/20220719153447%21Roach_2022_MitoFit.pdf doi:10.26124/mitofit:2022-0023.v1] - [https://wiki.oroboros.at/index.php/File:Roach_2022_MitoFit.pdf »Link to all versions«][[Roach 2022 Abstract Bioblast]]: Tolerance of rapid changes in light intensity by photosynthetic organisms is facilitated by non-photochemical quenching (NPQ), a term with reference to quenching of chlorophyll fluorescence, the technique used in its discovery. Mechanisms of NPQ include dissipating excess light energy to heat (qE), the reversible attachment of light-harvesting complexes (LHC) to photosystems (state transition / qT) and photoinhibition (qI). Chlorophyll is a ubiquitous pigment of photosynthetic organisms, found in LHC and the reaction centres of photosystem II and I (PSII; PSI). At room temperature, pulse-amplitude modulated (PAM) chlorophyll fluorescence protocols provide insights into PSII efficiency, thus a reasonable proxy for photosynthetic activity (carbon fixation), at least under optimal conditions. NPQ has a major impact on chlorophyll fluorescence intensity and is also quantified by PAM. Since NPQ mechanisms can occur simultaneously, they cause complexities in deciphering the signal. In algae, the ability for chlorophyll fluorescence in determining photosynthetic rates is not perfect, but it can still provide valuable information of processes affecting light harvesting. The aim of this report is to provide an overview of how various NPQ mechanisms in the model unicellular chlorophyte alga, ''Chlamydomonas reinhardtii'', as well as environmental conditions, affect chlorophyll fluorescence. I also propose a PAM protocol enabling the kinetics associated with each of the NPQ phases to be semi-quantified in under 20 min. h of the NPQ phases to be semi-quantified in under 20 min. )
Di Marcello 2019 MitoFit Preprint Arch EA + ( ::: Version 3 ('"v3"') '''20 … ::: Version 3 ('"v3"') '''2019-07-03''' [https://www.mitofit.org/images/1/15/Di_Marcello_2019_MitoFit_Preprint_Arch_doi_10.26214mitofitea19.MiPSchool.0005.v2.pdf doi:10.26124/mitofit:ea19.MiPSchool.0005.v2.pdf]::: Version 2 (v2) 2019-06-27 [https://www.mitofit.org/images/1/15/Di_Marcello_2019_MitoFit_Preprint_Arch_doi_10.26214mitofitea19.MiPSchool.0005.v2.pdf doi:10.26124/mitofit:ea19.MiPSchool.0005.v2.pdf]::: Version 1 (v1) 2019-06-15 [http://www.mitofit.org/images/0/09/Di_Marcello_2019_MitoFit_Preprint_Arch.pdf doi:10.26124/mitofit:ea19.MiPSchool.0005]Bioenergetics is the study of how living organisms acquire and transform energy to perform biological work. Energetic coupling between chloroplasts and mitochondria has been described in algae, demonstrating the good functionality and interaction between both organelles is necessary to maintain metabolic integrity. High-resolution respirometry (HRR) is widely used to assess mitochondrial respiration and other bioenergetics parameters in the biomedical field of mitochondrial research and its clinical applications. In our interdisciplinary study, we adapted the multimodal approach of the Oroboros O2k high-resolution respirometer to investigate algal bioenergetics for biotechnological purposes. - ''Extended abstract''gate algal bioenergetics for biotechnological purposes. - ''Extended abstract'' )
Pallag 2022 MitoFit Proline + ( ::: Version 3 ('''v3''') ''' … ::: Version 3 ('''v3''') '''2022-03-07''' [https://wiki.oroboros.at/images/4/42/Pallag_2022_MitoFit_Proline.pdf doi:10.26124/mitofit:2022-0001.v3]::: Version 2 (v2) 2022-03-03 [https://wiki.oroboros.at/images/archive/4/42/20220307085642%21Pallag_2022_MitoFit_Proline.pdf doi:10.26124/mitofit:2022-0001.v2]::: Version 1 (v1) 2022-03-02 [https://wiki.oroboros.at/images/archive/4/42/20220303104356%21Pallag_2022_MitoFit_Proline.pdf doi:10.26124/mitofit:2022-0001] - [https://wiki.oroboros.at/index.php/File:Pallag_2022_MitoFit_Proline.pdf »Link to all versions«]In mitochondria expressing proline dehydrogenase (ProDH), oxidation of proline to pyrroline-5-carboxylate (P5C) leads to transfer of electrons to ubiquinone supporting Complexes CIII and CIV, in turn generating the protonmotive force. Further catabolism of P5C forms glutamate that fuels the citric acid cycle yielding reducing equivalents sustaining oxidative phosphorylation. However, P5C and glutamate catabolism depend on CI activity due to NAD+ requirement. The extent of proline oxidation was established in isolated mitochondria of various mouse tissues by means of simultaneously measuring oxygen consumption, membrane potential, NADH and ubiquinone redox state using the NextGen-O2k (Oroboros Instruments) and correlated to ProDH activity and F1FO-ATPase directionality. In CI-inhibited mouse liver and kidney mitochondria exhibiting high levels of proline oxidation and ProDH activity, catabolism of proline generated a sufficiently high membrane potential maintaining F1FO-ATPase operation in forward mode. This was not observed when either CIII or CIV was inhibited, nor during anoxia. Fueling CIII and CIV with duroquinone partially reproduced the effects of proline. Excess glutamate could not reproduce the effects of proline, arguing that they are due to processes upstream of glutamate conversion from proline. The ProDH inhibitors L-tetrahydro-2-furoic acid and to lesser extent S-5-oxo-2-tetrahydrofurancarboxylic acid abolished all effects conferred by proline. It is concluded that proline catabolism through ProDH generates sufficient CIII and CIV proton pumping, supporting ATP production by F1FO-ATPase even when CI is inhibited. production by F1FO-ATPase even when CI is inhibited. )
Gnaiger 2021 MitoFit BCA + ( ::: Version 1 ('''v1''') '''2021-09-21''' … ::: Version 1 ('''v1''') '''2021-09-21''' [https://www.mitofit.org/images/1/16/Gnaiger_2021_MitoFit_BCA.pdf doi:10.26124/mitofit:2021-0008][[File:Gnaiger 2021 MitoFit BCA-graphical abstract.png|right|300px|Graphical abstract]]Cell respiration reflects mitochondrial fitness and plays a pivotal role in health and disease. Despite the rapidly increasing number of applications of cell respirometry to address current challenges in biomedical research, cross-references are rare between respirometric projects and platforms. Evaluation of accuracy and reproducibility between laboratories requires presentation of results in a common format independent of the applied method. When cell respiration is expressed as oxygen consumption rate in an experimental chamber, normalization is mandatory for comparability of results. Concept-driven normalization and regression analysis are key towards bioenergetic cluster analysis presented as a graphical tool to identify discrete data populations.In a meta-analysis of human skin fibroblasts, high-resolution respirometry and polarography covering cell senescence and the human age range are compared with multiwell respirometry. The common coupling control protocol measures ROUTINE respiration of living cells followed by sequential titrations of oligomycin, uncoupler, and inhibitors of electron transfer.Bioenergetic cluster analysis increases the resolution of outliers within and differences between groups. An outlier-skewness index is introduced as a guide towards logarithmic transformation for statistical analysis. Isolinear clusters are separated by variations in the extent of a quantity that correlates with the rate, whereas heterolinear clusters fall on different regression lines. Dispersed clusters are clouds of data separated by a critical threshold value. Bioenergetic cluster analysis provides new insights into mitochondrial respiratory control and a guideline for establishing a quality control paradigm for bioenergetics and databases in mitochondrial physiology. bases in mitochondrial physiology. )
Donnelly 2022 MitoFit Hypoxia + ( ::: Version 2 ('''v2''') '''2022-07-15''' … ::: Version 2 ('''v2''') '''2022-07-15''' [https://wiki.oroboros.at/images/4/44/Donnelly_2022_MitoFit_Hypoxia.pdf The ABC of hypoxia – what is the norm https://doi.org/10.26124/mitofit:2022-0025.v2]::: Version 1 (v1) 2022-06-28 - [https://wiki.oroboros.at/index.php/File:Donnelly_2022_MitoFit_Hypoxia.pdf »Link to all versions«][[File:Oxia terms.png|right|250px]][[Donnelly 2022 Abstract Bioblast]]: Hypoxia is a condition of oxygen levels below normoxia and opposite to hyperoxia. We here define the normoxic reference state by three complementary precepts: ('''A''') ambient normoxia at sea level in the contemporary atmosphere and corresponding dissolved O2 concentration at air saturation of aqueous environments; ('''B''') biological compartmental O2 levels at ambient normoxia under physiological activity of healthy organisms in the absence of environmental stress (e.g. in a diving human, a stranded whale, a thermally stressed animal); and ('''C''') O2 levels above the control region, i.e., where the capacity for O2 consumption is not compromised by partial O2 pressure as evaluated by its kinetics. Conversely, the '''abc''' of hypoxia is concerned with deviations from these reference points caused by different mechanisms: ('''a''') ambient alterations of oxygen levels; ('''b''') biological O2 demand exceeding O2 supply under pathological or experimental limitations of convective O2 transport or O2 diffusion; and ('''c''') critical oxygen pressure in oxygen kinetics shifted by pathological and toxicological effects or environmental stress. The ABC of hypoxia may be of help in the design and interpretation of ''in vitro'' and ''in vivo'' experimental studies. ical effects or environmental stress. The ABC of hypoxia may be of help in the design and interpretation of ''in vitro'' and ''in vivo'' experimental studies. )
Cardoso 2021 MitoFit MgG + (<big>'''Journal publication 2021-06- … <big>'''Journal publication 2021-06-30 in [https://www.bioenergetics-communications.org/index.php/bec/article/view/cardoso_2021_mgg »Bioenergetics Communications 2021.1«]'''</big>For the advanced study of mitochondrial function, high-resolution respirometry is extended by fluorometric measurement of ATP production using the fluorophore Magnesium Green™ (MgG). A common problem with several fluorescent dyes is the inhibition of mitochondrial respiration. In the present study, a coupling control protocol was applied in combination with MgG to measure ATP production simultaneously with respiration for calculation of P»/O2 ratios. MgG at 1.1 µM did not affect respiration through the NADH-linked and succinate-linked pathways. Respiration was not inhibited in any of the coupling control states, hence coupling control efficiencies were not affected by MgG.tes, hence coupling control efficiencies were not affected by MgG.)
Krako Jakovljevic 2021 MitoFit PD + (<big>'''Journal publication 2021-10- … <big>'''Journal publication 2021-10-06 in [https://www.bioenergetics-communications.org/index.php/bec/article/view/krako_jakovljevic_2021_pd »Bioenergetics Communications 2021.2«]'''</big>Mitochondrial function is known to be an important factor in maintaining cellular homeostasis and its dysregulation has become a hallmark for multiple disease conditions. This review aims to synthesise the extent of this knowledge by analysing changes of mitochondrial physiology parameters in Parkinson’s disease (PD) and to evaluate the contribution of cellular models of PD in the field. The analysis provided here constitutes a platform for further elucidation of mitochondrial function parameters relative to factors that may potentiate disease progression.ve to factors that may potentiate disease progression.)
Vernerova 2021 MitoFit PLT + (<big>'''Journal publication 2021-12- … <big>'''Journal publication 2021-12-08 in [[Vernerova 2021 Biomedicines |''Biomedicines'']]'''</big>[[File:Vernerova 2021 Mitofit PLT - graphical abstract.png|right|300px|Graphical abstract]] Multiple non-aggregatory functions of human platelets (PLT) are widely acknowledged, yet their functional examination is limited mainly due to a lack of standardized isolation and analytic methods. Platelet apheresis (PA) is an established clinical method for PLT isolation aiming at the treatment of bleeding diathesis in severe thrombocytopenia. On the other hand, density gradient centrifugation (DC) is an isolation method applied in research for the analysis of the mitochondrial metabolic profile of oxidative phosphorylation (OXPHOS) in PLT obtained from small samples of human blood. We studied PLT obtained from 29 healthy donors by high-resolution respirometry for comparison of PA and DC isolates. ROUTINE respiration and electron transfer capacity of living PLT isolated by PA were significantly higher than in the DC group, whereas plasma membrane permeabilization resulted in a 57 % decrease of succinate oxidation in PA compared to DC. These differences were eliminated after washing the PA cells with phosphate buffer containing 10 mmol·L-1 EGTA, suggesting that several components, particularly Ca2+ and fuel substrates, were carried over into the respiratory assay from the serum in PA. A simple washing step was sufficient to enable functional mitochondrial analysis in subsamples obtained from PA.The combination of the standard clinical PA isolation procedure with PLT quality control and routine mitochondrial OXPHOS diagnostics meets an acute clinical demand in biomedical research of patients suffering from thrombocytopenia and metabolic diseases. h of patients suffering from thrombocytopenia and metabolic diseases. )
Komlodi 2021 MitoFit AmR-O2 + (<big>'''Journal publication 2021-12- … <big>'''Journal publication 2021-12-21 in [https://www.bioenergetics-communications.org/index.php/bec/article/view/komlodi_2021_amr »Bioenergetics Communications 2021.4«]'''</big>[[File:Komlodi 2021 MitoFit AmR-O2 graphical abstract.png|right|300px|Graphical abstract]]The fluorometric Amplex UltraRed AmR assay is frequently used for quantitative assessment of hydrogen peroxide production. It is specific to H2O2, can be calibrated accurately, and allows continuous real-time measurement. Without correction for the background fluorescence slope, however, H2O2-independent formation of the fluorescent product UltroxRed (or resorufin) leads to artefacts.We analysed (''1'') the medium specificity of the background fluorescence slope of the AmR assay, and (''2'') the oxygen dependence of H2O2 flux in baker´s yeast ''Saccharomyces cerevisiae''. Apparent H2O2 flux, O2 concentration and O2 flux were measured simultaneously by high-resolution respirometry equipped with the fluorescence module. The apparent H2O2 flux of yeast showed a maximum under hypoxia when incubated in Dulbecco´s Phosphate Buffered Saline DPBS or KCl-medium. This hypoxic peak increased with the sequential number of normoxic-anoxic transitions. Even in the absence of yeast, the fluorescence slope increased at low O2 levels as a function of fluorescence intensity. The hypoxic peak was not observed in mitochondrial respiration medium MiR05.Therefore, the hypoxic peak was a medium-specific background effect unrelated to cell physiology. In MiR05, H2O2 production of yeast decreased linearly from hyperoxia to hypoxia, with a steep decline towards anoxia. Respiration and oxygen dependence expressed as ''p''50 of yeast were higher in MiR05 than DPBS. Respiration was a hyperbolic function of oxygen concentration in the low-oxygen range. The flux-dependence of oxygen affinity explained the higher ''p''50 in MiR05. /sub> of yeast were higher in MiR05 than DPBS. Respiration was a hyperbolic function of oxygen concentration in the low-oxygen range. The flux-dependence of oxygen affinity explained the higher ''p''50 in MiR05. )
Buck 2013 Abstract MiP2013 + (<big>'''Peter Hochachka lecture'''&l … <big>'''Peter Hochachka lecture'''</big>Earth’s changing environment has been a major evolutionary force shaping the diversity of species both in the past and present. In particular, seasonal ice cover in northern latitudes has selected for hypoxia and anoxia tolerance in some species, such as freshwater turtles. At the northern reaches of their range North American western painted turtles spend 4 months or more buried in the mud bottom of ice covered lakes and ponds [1]. This offers a unique opportunity to understand how a vertebrate brain, an organ extremely sensitive to reduced oxygen availability in mammals, can function without oxygen [2]. Through oxidative phosphorylation mitochondria fuel the inherently high energetic demands of brain and in mammals mitochondria also play a key role in injury from hypoxic stress – including loss of calcium homeostasis and production of reactive oxygen species (ROS) leading to apoptosis and necrosis. Hypoxic or anoxic stress does not signal stress in turtle brain but rather protective mechanisms with the onset of anoxia. Indeed our data show that mitochondria play a key role in low oxygen signaling in turtle brain by a reduction in mitochondrial membrane potential and release of a relatively small but significant amount of calcium. The increase in cytosolic calcium signals a phosphatase based mechanism to decrease whole-cell glutamatergic (NMDA and AMPA) excitatory currents in pyramidal neurons. While in stellate neurons anoxia results in a large reduction in mitochondrial ROS production that increases the magnitude of GABAergic inhibitory neurotransmission. The increased GABA activity produces a chloride based shunting current that “arrests” action potentials in pyramidal cells resulting in metabolic depression and neuroprotection.resulting in metabolic depression and neuroprotection.)
Weber 2013 Abstract MiP2013 + (<big>'''[[Johansen K|Kjell Johansen]] … <big>'''[[Johansen K|Kjell Johansen]] lecture'''</big>Vertebrate hemoglobins (Hb) are exquisitely designed to transport O2 from the respiratory organs to the tissues, thereby safeguarding mitochondrial O2 supply and aerobic metabolism in the face of wide and independent variations in O2 tensions and temperature at the sites for loading and unloading of O2 [1-3]. In transporting O2, vertebrate Hbs (composed of 2 α and 2 β globin chains) switch between the T (tense, low O2-affinity, deoxygenated) structure that predominates in the tissues, and the R (relaxed, high-affinity, oxygenated) structure that predominates in the lungs and gills. The T-R shift is basic to cooperativity between the O2-binding heme groups that increases O2 (un)loading for a given change in O2 tension - and is reflected in the sigmoid shape of O2 binding curves. Hb’s in vivo O2 binding properties are a product of its intrinsic O2 affinity and its interaction with red cell allosteric effectors that decreases Hb-O2 affinity by stabilizing the T-structure. Apart from protons and CO2 (that facilitate O2 unloading in the acid tissues via the “Bohr-effect”) these effectors include chloride ions and organic phosphates [ATP in lower vertebrates, IPP (inositol pentaphosphate) in birds and DPG (diphosphoglycerate) in mammals]. The interaction with effectors varies between and within individual species and plays a key role in adjusting O2 transport in response to changes in environmental conditions, metabolic requirements, and mode of life. The decrease in Hb-O2 affinity with rising temperature mandated by the exothermic nature of heme oxygenation, enhances O2 unloading in warm tissues that require more O2, but may become maladaptive – and thus commonly is reduced - in regional heterothermic species where it may hamper O2 unloading (in cold extremities of arctic mammals) or cause excessive O2 release (in warm muscles, brains or eyes of fast-swimming fish).Based on case studies (Hbs from estivating fish, fast-swimming gamefish, high-altitude Andean frogs, geese that scale the Himalayas, Rocky Mountain Deer mice and Hb recreated from extinct mammoths [4-6]) the treatise analyses the molecular mechanisms for Hb’s role in securing mitochondrial O2 supply under stressful conditions - illustrating the key significance of molecular interactions to understanding physiological ecology. of molecular interactions to understanding physiological ecology.)
Walker 2013 Abstract MiP2013 + (<big>MiP2013 Keynote by Sir John Wal … <big>MiP2013 Keynote by Sir John Walker</big>The lecture will be devoted to the topic of how the biological world supplies itself with energy to make biology work, and what medical consequences ensue when the energy supply chain in our bodies is damaged or defective. We derive our energy from sunlight, which, via photosynthesis in green plants, provides high energy components in the foods that we ingest. We harvest that energy, effectively by “burning” (oxidising) the high energy components, releasing cellular energy in a controlled way to generate the fuel of life, in the form of the molecule known as adenosine triphosphate (or ATP for short). The key steps in this process take place in the mitochondria inside the cells that make up our tissues. They serve as biological “power stations” that contain millions of tiny molecular turbines, the ATP synthase, that rotate rather like man-made turbines churning out the cellular fuel in massive quantities, which is then delivered to all parts of our bodies to provide the energy to make them function. Each of us makes and expends about 60 kg of this fuel every day of our lives. Defects in the fuel supply process are increasingly being recognised as important components of complex human diseases such as cancer, neurodegeneration and neuromuscular diseases, and they may also be part of the process of ageing. The ATP synthases found in mitochondria, eubacteria and chloroplasts have many common features. Their overall architectures are similar, and they all consist of two rotary motors linked by a stator and a flexible rotor. When rotation of the membrane bound rotor is driven by proton motive force, the direction of rotation ensures that ATP is made from ADP and phosphate in the globular catalytic domain. When ATP serves as the source of energy and is hydrolysed in the catalytic domain, the rotor turns in the opposite sense and protons are pumped outwards through the membrane domain, and away from the catalytic domain. The lecture will describe the common features of their catalytic mechanisms. However, the ATP synthase from mitochondria, eubacteria and chloroplasts differ most fundamentally in the energy cost that is paid to make each ATP molecule. The most efficient ATP synthase is found in the mitochondria from multicellular animals. The ATP synthases in unicellular organisms, and chloroplasts, pay various higher costs that seem to reflect the supply of available energy in the biological niches that they inhabit. The ATP synthases also differ significantly in the way they are regulated. Eubacteria have evolved a range of mechanisms of regulation, and the chloroplast enzyme is rendered inactive by a redox mechanism in the hours darkness. Mitochondria contain an inhibitor protein, IF1, that inhibits ATP hydrolysis but not ATP synthesis. Its in vitro mechanism has been studied in great detail, but its in vivo role is mysterious, and suppression of expression of the protein appears not to influence respiration.In mitochondria the ATP synthase is organised in rows of dimers along the edges of the cristae, and as will be discussed, it has been suggested that the permeability transition pore involved in apoptosis resides in the dimeric enzyme.e involved in apoptosis resides in the dimeric enzyme.)
Lemieux 2017 bioRxiv 103457 + ( '''Lemieux H, Blier PU, Gnaig … '''Lemieux H, Blier PU, Gnaiger E (2017) Remodeling pathway control of mitochondrial respiratory capacity by temperature in mouse heart: electron flow through the Q-junction in permeabilized fibers. Sci Rep 7:2840, DOI:10.1038/s41598-017-02789-8.''' - [[Lemieux 2017 Sci Rep |»Bioblast link«]]* Accepted for publication: 2017-04-18* [http://rdcu.be/tgpY Sci Rep Open Access]: 2017-06-06://rdcu.be/tgpY Sci Rep Open Access]: 2017-06-06)
OroDM01 Innsbruck AT + ( '''Oroboros Distributor Meeting'''. Innsbruck, Austria; 2019 Jul 01-03.)
2nd Oroboros distributor training 2023 Innsbruck AT + ( '''Oroboros distributor training'''. Innsbruck, Austria; 2023 Nov 07-09.)
Oroboros distributor training 2023 Innsbruck AT + ( '''Oroboros distributor training'''. Innsbruck, Austria; 2023 Apr 24-25.)
MiP2015 Book of Abstracts Open Access + ( : » [[MiP2015]] - all abstracts in alphabetical order and programme sessions. : » [[MiP2015 Abstracts in the MiPMap]] - sort by MiP''areas'', species, tissues, diseases, ...)
Chung 2005 Am J Physiol Cell Physiol + (1H-NMR experiments … 1H-NMR experiments have determined intracellular O2 consumption (''V''O2) with oxymyoglobin (MbO2) desaturation kinetics in human calf muscle during plantar flexion exercise at 0.75, 0.92, and 1.17 Hz with a constant load. At the onset of muscle contraction, myoglobin (Mb) desaturates rapidly. The desaturation rate constant of approximately 30 s reflects the intracellular ''V''O2. Although Mb desaturates quickly with a similar time constant at all workload levels, its final steady-state level differs. As work increases, the final steady-state cellular ''P''O2 decreases progressively. After Mb desaturation has reached a steady state, however, ''V''O2 continues to rise. On the basis of current respiratory control models, the analysis in the present report reveals two distinct ''V''O2 phases: an ADP-independent phase at the onset of contraction and an ADP-dependent phase after Mb has reached a steady state. In contrast to the accepted view, the initial intracellular ''V''O2 shows that oxidative phosphorylation can support up to 36 % of the energy cost, a significantly higher fraction than expected. Partitioning of the energy flux shows that a 31 % nonoxidative component exists and responds to the dynamic energy utilization-restoration cycle (which lasts for only milliseconds) as postulated in the glycogen shunt theory. The present study offers perspectives on the regulation of respiration, bioenergetics, and Mb function during muscle contraction.ration cycle (which lasts for only milliseconds) as postulated in the glycogen shunt theory. The present study offers perspectives on the regulation of respiration, bioenergetics, and Mb function during muscle contraction.)
Cohn 1953 J Biol Chem + (A new reaction which occurs in oxida … A new reaction which occurs in oxidative phosphorylation associated with the electron transport system has been observed in rat liver mitochondria with α-ketoglutarate, β-hydroxybutyrate, and succinate as substrates. This reaction manifests itself by a replacement of O18 with normal oxygen in inorganic phosphate labeled with O18 and parallels the phosphorylation which is associated with the oxidation. The number of molecules of inorganic phosphate which participate in this reaction, calculated on the basis that a monoester of phosphate is involved, is several times higher than the number of high energy phosphate bonds that can be formed. The reaction does not occur at the substrate level oxidation of α-ketoglutarate and the evidence suggests that it occurs at every step in the electron transport system. This phosphate turnover reaction occurs only when phosphorylation is proceeding. Dinitrophenol suppresses the reaction. The omission of Mg++ or adenylic acid also suppresses the reaction. The reaction is abolished when succinate oxidation is catalyzed by a succinic oxidase preparation containing no phosphorylating system. The possibility that the reaction is due to a direct reaction of ATP, hydrolytic or otherwise, is eliminated. Various mechanisms which are consistent with the findings are discussed.stent with the findings are discussed.)
Kielley 1951 J Biol Chem + (A simplified procedure for preparing … A simplified procedure for preparing mitochondria suspensions from isotonic sucrose homogenates has been described. These preparations exhibit high rates of net 7 minute phosphorus formation from adenylic acid during the oxidation of α-ketoglutarate in the absence of inhibitors such as fluoride, and show very low dephosphorylating activities. It has been possible to study the complete phosphorylation of AMP in this system and to interpret the characteristics of this process on the basis of adenosinediphosphate as primary phosphate acceptor and the presence of a myokinase in mitochondria. The activity of this transphosphorylase has been directly determined and is of considerable magnitude. It has also been demonstrated that probably all of the myokinase is associated with the mitochondrial fraction. The changes in the characteristics of oxidative phosphorylation and adenosinetriphosphatase activity as the result of incubation of the enzyme at 28° in the absence of substrates have been studied. The inactivation of the phosphorylation system by aging has been considered in two phases, an initial lag phase which is completely reversible in short aging experiments and a permanent reduction in activity observed with more severely aged mitochondria. The initial very low ATPase activity of the mitochondria was increased to appreciable magnitudes by aging. All the characteristics of aging were prevented to a large extent by AMP, ADP, or ATP. a large extent by AMP, ADP, or ATP.)
Chance 1961 J Biol Chem-I + (A thermodynamically improbable reductio … A thermodynamically improbable reduction of pyridine nucleotide caused by the addition of succinate to isolated mitochondria has been demonstrated. The material so reduced exhibits kinetic responses, some of which can suggest its consideration as a member of the respiratory chain, but a quantitative examination of the kinetics of oxidation and reduction shows that only a small portion of the total respiratory activity in succinate oxidation passes through the diphosphopyridine nucleotide-linked pathway. The nature of the reduction product has been examined in heart, liver, and guinea pig kidney mitochondria and is found to be material absorbing at 340 mµ and having a fluorescence emission maximum at 440 mµ. Direct chemical assays on kidney mitochondria indicate that the reduced material is diphosphopyridine nucleotide. A preliminary evaluation of various hypotheses to explain this result leads us tentatively to reject hypotheses based upon a single pool of mitochondrial pyridine nucleotide in which diphosphopyridine nucleotide and succinate compete for oxidizing equivalents from the cytochrome chain. Further indication of the complexities of this reaction is that respiration can be initiated by succinate without measurable pyridine nucleotide reduction and that a transition from aerobiosis in state 3 to anaerobiosis (state 5) can lead to a higher oxidation level of pyridine nucleotide than was observed aerobically in state 4. These observations suggest that the presence of adenosine 5’-diphosphate inhibits pyridine nucleotide reduction under both aerobic and anaerobic conditions and support the possibility that an energy-linked reaction may be involved.nergy-linked reaction may be involved.)
Pesta 2011Abstract Mitochondrial Medicine-Diagnosis + (A 28-year-old former amateur cyclist demon … A 28-year-old former amateur cyclist demonstrated a sudden exercise intolerance and impairment in muscle function since March 2008 without clinical explanation. The main symptom was a decreased ergometric aerobic capacity by 50%. A specific defect of mitochondrial glutamate dehydrogenase (GDH) was indicated by lack of ADP stimulation in the presence of glutamate and subsequent rescue of respiration after addition of malate.e of respiration after addition of malate.)
Kancirova 2016 Physiol Res + (A 2×2 factorial design was used to evaluat … A 2×2 factorial design was used to evaluate possible preservation of mitochondrial functions in two cardioprotective experimental models, remote ischemic preconditioning and streptozotocin-induced ''diabetes mellitus'', and their interaction during ischemia/reperfusion injury (I/R) of the heart. Male Wistar rats were randomly allocated into four groups: control (C), streptozotocin-induced diabetic (DM), preconditioned (RPC) and preconditioned streptozotocin-induced diabetic (DM+RPC). RPC was conducted by 3 cycles of 5-min hind-limb ischemia and 5-min reperfusion. DM was induced by a single dose of 65 mg/kg streptozotocin. Isolated hearts were exposed to ischemia/reperfusion test according to Langendorff. Thereafter mitochondria were isolated and the mitochondrial respiration was measured. Additionally, the ATP synthase activity measurements on the same preparations were done. Animals of all groups subjected to I/R exhibited a decreased state 3 respiration with the least change noted in DM+RPC group associated with no significant changes in state 2 respiration. In RPC, DM and DM+RPC group, no significant changes in the activity of ATP synthase were observed after I/R injury. These results suggest that the endogenous protective mechanisms of RPC and DM do preserve the mitochondrial function in heart when they act in combination.ion in heart when they act in combination.)
Gaudo 2019 Neurogenetics + (A 3-year-old girl presented with severe ep … A 3-year-old girl presented with severe epilepsy in the context of ''Borrelia'' infection. After ceftriaxone/lidocaine administration, she showed secondarily generalized focal crises that led to neurological and motor sequelae. Genetic studies identified in the patient two heterozygous POLG mutations (c.2591A>G; p.Asn864Ser and c.3649G>C; p.Ala1217Pro). Through analysis of POLG activity in cultured fibroblasts, we confirmed that the mutations altered the mtDNA turnover. Moreover, patient fibroblasts were more sensitive than controls in the presence of a mitochondrial replication-affecting drug, the antiretroviral azidothymidine. To test if ceftriaxone treatment could worsen the deleterious effect of the patient mutations, toxicity assays were performed. Cell toxicity, without direct effect on mitochondrial respiratory function, was detected at different antibiotic concentrations. The clinical outcome, together with the different ''in vitro'' sensitivity to ceftriaxone among patient and control cells, suggested that the mitochondrial disease symptoms were hastened by the infection and were possibly worsened by the pharmacological treatment. This study underscores the benefit of early genetic diagnosis of the patients with mitochondrial diseases, since they may be a target group of patients especially vulnerable to environmental factors. especially vulnerable to environmental factors.)
Nijholt 2023 Sci Rep + (A Kinase Interacting Protein 1 (AKIP1) is … A Kinase Interacting Protein 1 (AKIP1) is a signalling adaptor that promotes mitochondrial respiration and attenuates mitochondrial oxidative stress in cultured cardiomyocytes. We sought to determine whether AKIP1 influences mitochondrial function and the mitochondrial adaptation in response to exercise ''in vivo''. We assessed mitochondrial respiratory capacity, as well as electron microscopy and mitochondrial targeted-proteomics in hearts from mice with cardiomyocyte-specific overexpression of AKIP1 (AKIP1-TG) and their wild type (WT) littermates. These parameters were also assessed after four weeks of voluntary wheel running. In contrast to our previous ''in vitro'' study, respiratory capacity measured as state 3 respiration on palmitoyl carnitine was significantly lower in AKIP1-TG compared to WT mice, whereas state 3 respiration on pyruvate remained unaltered. Similar findings were observed for maximal respiration, after addition of FCCP. Mitochondrial DNA damage and oxidative stress markers were not elevated in AKIP1-TG mice and gross mitochondrial morphology was similar. Mitochondrial targeted-proteomics did reveal reductions in mitochondrial proteins involved in energy metabolism. Exercise performance was comparable between genotypes, whereas exercise-induced cardiac hypertrophy was significantly increased in AKIP1-TG mice. After exercise, mitochondrial state 3 respiration on pyruvate substrates was significantly lower in AKIP1-TG compared with WT mice, while respiration on palmitoyl carnitine was not further decreased. This was associated with increased mitochondrial fission on electron microscopy, and the activation of pathways associated with mitochondrial fission and mitophagy. This study suggests that AKIP1 regulates the mitochondrial proteome involved in energy metabolism and promotes mitochondrial turnover after exercise. Future studies are required to unravel the mechanistic underpinnings and whether the mitochondrial changes are required for the AKIP1-induced physiological cardiac growth.KIP1-induced physiological cardiac growth.)