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A list of all pages that have property "Has abstract" with value "2nd Mitochondria Conference, Lisbon, Portugal, 2023.". Since there have been only a few results, also nearby values are displayed.

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  • 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 Additionally, 3-BrPA treatment significantly impaired lactate production by HepG2 cells, even when glucose was withdrawn from the incubation medium.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 ag3-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 (Ca<sup>2+</sup>) 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, Ca<sup>2+</sup>-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 ag3-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 (HMG3-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<sup>th</sup> 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<sup>rd</sup> MiP''summer school'' on Mitochondrial Respiratory Physiology, 2009 June 17-23, Baton Rouge, Louisiana US.)
  • Eugeny I. Schwartz Conference 2015  + (3<sup>rd</sup> 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;)