224 results on '"Muntean, Danina M."'
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2. Empagliflozin and dapagliflozin decreased atrial monoamine oxidase expression and alleviated oxidative stress in overweight non-diabetic cardiac patients
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Ionică, Loredana N., Buriman, Darius G., Lința, Adina V., Șoșdean, Raluca, Lascu, Ana, Streian, Caius G., Feier, Horea B., Petrescu, Lucian, Mozoș, Ioana M., Sturza, Adrian, and Muntean, Danina M.
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- 2024
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3. Vascular Toxicity of Endocrine Disruptors: A Thinly Veiled Threat
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Muntean, Danina M., Linţa, Adina V., Ionică, Loredana N., Dănilă, Maria D., Lighezan, Daniel F., Sturza, Adrian, Dhalla, Naranjan S., Series Editor, Bolli, Roberto, Editorial Board Member, Goyal, Ramesh, Editorial Board Member, Kartha, Chandrasekharan, Editorial Board Member, Kirshenbaum, Lorrie, Editorial Board Member, Makino, Naoki, Editorial Board Member, Mehta, Jawahar L. L., Editorial Board Member, Ostadal, Bohuslav, Editorial Board Member, Pierce, Grant N., Editorial Board Member, Slezak, Jan, Editorial Board Member, Varro, Andras, Editorial Board Member, Werdan, Karl, Editorial Board Member, Weglicki, William B., Editorial Board Member, Djuric, Dragan M., editor, and Agrawal, Devendra K., editor
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- 2024
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4. Metformin and empagliflozin modulate monoamine oxidase-related oxidative stress and improve vascular function in human mammary arteries
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Lascu, Ana, Ionică, Loredana N., Buriman, Darius G., Merce, Adrian P., Deaconu, Loredana, Borza, Claudia, Crețu, Octavian M., Sturza, Adrian, Muntean, Danina M., and Feier, Horea B.
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- 2023
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5. Monoamine oxidase is a source of cardiac oxidative stress in obese rats: the beneficial role of metformin
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Merce, Adrian P., Ionică, Loredana N., Bînă, Anca M., Popescu, Simona, Lighezan, Rodica, Petrescu, Lucian, Borza, Claudia, Sturza, Adrian, Muntean, Danina M., and Creţu, Octavian M.
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- 2023
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6. Placental oxidative stress and monoamine oxidase expression are increased in severe preeclampsia: a pilot study
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Bînă, Anca M., Sturza, Adrian, Iancu, Ioana, Mocanu, Adelina G., Bernad, Elena, Chiriac, Daniela V., Borza, Claudia, Craina, Marius L., Popa, Zoran L., Muntean, Danina M., and Crețu, Octavian M.
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- 2022
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7. Impairment of mitochondrial respiration in platelets and placentas: a pilot study in preeclamptic pregnancies
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Bînă, Anca M., Aburel, Oana M., Avram, Vlad F., Lelcu, Theia, Lința, Adina V., Chiriac, Daniela V., Mocanu, Adelina G., Bernad, Elena, Borza, Claudia, Craina, Marius L., Popa, Zoran L., Muntean, Danina M., and Crețu, Octavian M.
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- 2022
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8. Monoamine Oxidase, Obesity and Related Comorbidities: Discovering Bonds
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Sturza, Adrian, Muntean, Danina M., Crețu, Octavian M., Dhalla, Naranjan S., Series Editor, Bolli, Roberto, Editorial Board Member, Goyal, Ramesh, Editorial Board Member, Kartha, Chandrasekharan, Editorial Board Member, Kirshenbaum, Lorrie, Editorial Board Member, Makino, Naoki, Editorial Board Member, Mehta, Jawahar L. L., Editorial Board Member, Ostadal, Bohuslav, Editorial Board Member, Pierce, Grant N., Editorial Board Member, Slezak, Jan, Editorial Board Member, Varro, Andras, Editorial Board Member, Werdan, Karl, Editorial Board Member, Weglicki, William B., Editorial Board Member, Tappia, Paramjit S., editor, and Ramjiawan, Bram, editor
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- 2021
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9. Metformin alleviates monoamine oxidase-related vascular oxidative stress and endothelial dysfunction in rats with diet-induced obesity
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Ionică, Loredana N., Gaiță, Laura, Bînă, Anca M., Soșdean, Raluca, Lighezan, Rodica, Sima, Alexandra, Malița, Daniel, Crețu, Octavian M., Burlacu, Ovidiu, Muntean, Danina M., and Sturza, Adrian
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- 2021
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10. The Off-Target Cardioprotective Mechanisms of Sodium–Glucose Cotransporter 2 Inhibitors: An Overview.
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Ionică, Loredana N., Lința, Adina V., Bătrîn, Alina D., Hâncu, Iasmina M., Lolescu, Bogdan M., Dănilă, Maria D., Petrescu, Lucian, Mozoș, Ioana M., Sturza, Adrian, and Muntean, Danina M.
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SODIUM-glucose cotransporter 2 inhibitors ,NEPRILYSIN ,BLOOD sugar ,HEART failure - Abstract
Sodium–glucose cotransporter 2 inhibitors (SGLT2i), a novel class of glucose-lowering drugs, have revolutionized the management of heart failure with reduced and preserved ejection fraction, regardless of the presence of diabetes, and are currently incorporated in the heart failure guidelines. While these drugs have consistently demonstrated their ability to decrease heart failure hospitalizations in several landmark clinical trials, their cardioprotective effects are far from having been completely elucidated. In the past decade, a growing body of experimental research has sought to address the molecular and cellular mechanisms of SGLT2i in order to provide a better understanding of the off-target acute and chronic cardiac benefits, beyond the on-target renal effect responsible for blood glucose reduction. The present narrative review addresses the direct cardioprotective effects of SGLT2i, delving into the off-target mechanisms of the drugs currently approved for heart failure therapy, and provides insights into future perspectives. [ABSTRACT FROM AUTHOR]
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- 2024
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11. Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.
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Lința, Adina V., Lolescu, Bogdan M., Ilie, Cosmin A., Vlad, Mihaela, Blidișel, Alexandru, Sturza, Adrian, Borza, Claudia, Muntean, Danina M., and Crețu, Octavian M.
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HEPATOTOXICOLOGY ,OXIDATIVE stress ,FATTY liver ,PANCREAS ,MITOCHONDRIA ,METABOLIC disorders - Abstract
In recent years, the worldwide epidemic of metabolic diseases, namely obesity, metabolic syndrome, diabetes and metabolic-associated fatty liver disease (MAFLD) has been strongly associated with constant exposure to endocrine-disruptive chemicals (EDCs), in particular, the ones able to disrupt various metabolic pathways. EDCs have a negative impact on several human tissues/systems, including metabolically active organs, such as the liver and pancreas. Among their deleterious effects, EDCs induce mitochondrial dysfunction and oxidative stress, which are also the major pathophysiological mechanisms underlying metabolic diseases. In this narrative review, we delve into the current literature on EDC toxicity effects on the liver and pancreatic tissues in terms of impaired mitochondrial function and redox homeostasis. [ABSTRACT FROM AUTHOR]
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- 2024
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12. Vitamin D alleviates oxidative stress in adipose tissue and mesenteric vessels from obese patients with subclinical inflammation
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Ionica, Mihaela, Aburel, Oana M., Vaduva, Adrian, Petrus, Alexandra, Ratiu, Sonia, Olariu, Sorin, Sturza, Adrian, and Muntean, Danina M.
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Medical research ,Medicine, Experimental ,Obesity ,Adipose tissues ,Inflammation ,Alfacalcidol ,Endothelium ,Calcifediol ,Vitamin D ,Oxidative stress ,C-reactive protein ,Type 2 diabetes ,Biological sciences - Abstract
Obesity is an age-independent, lifestyle-triggered, pandemic disease associated with both endothelial and visceral adipose tissue (VAT) dysfunction leading to cardiometabolic complications mediated via increased oxidative stress and persistent chronic inflammation. The purpose of the present study was to assess the oxidative stress in VAT and vascular samples and the effect of in vitro administration of vitamin D. VAT and mesenteric artery branches were harvested during abdominal surgery performed on patients referred for general surgery (n = 30) that were randomized into two subgroups: nonobese and obese. Serum levels of C-reactive protein (CRP) and vitamin D were measured. Tissue samples were treated or not with the active form of vitamin D: 1,25[(OH).sub.2][D.sub.3] (100 nmol/L, 12 h). The main findings are that in obese patients, (i) a low vitamin D status was associated with increased inflammatory markers and reactive oxygen species generation in VAT and vascular samples and (ii) in vitro incubation with vitamin D alleviated oxidative stress in VAT and vascular preparations and also improved the vascular function. We report here that the serum level of vitamin D is inversely correlated with the magnitude of oxidative stress in the adipose tissue. Ex vivo treatment with active vitamin D mitigated obesity-related oxidative stress. Key words: visceral adipose tissue, mesenteric arteries, oxidative stress, endothelial dysfunction. Resume : L'obesite est une maladie pandemique, independante de l'age et declenchee par le mode de vie qui est associee a des dysfonctionnements endotheliaux comme du tissu adipeux visceral (TAV) et qui mene a des complications cardiometaboliques mediees par l'intermediaire d'une augmentation du stress oxydatif et de la persistance d'une inflammation chronique. La presente etude visait a evaluer le stress oxydatif dans des echantillons de TAV et de vaisseaux, ainsi que l'effet de l'administration de vitamine D in vitro. Nous avons preleve du TAV et des rameaux d'artere mesenterique au cours d'interventions chirurgicales abdominales effectuees chez des patients diriges en chirurgie generale (n = 30), que nous avons repartis aleatoirement dans deux sous-groupes : non-obeses et obeses. Nous avons mesure les taux seriques de proteine C reactive et de vitamine D. Nous avons mis des echantillons de tissu en presence ou non de la forme active de la vitamine D--1,25[(OH).sub.2][D.sub.3] (100 nM, 12 h). Voici nos principaux resultats chez les patients obeses : (i) association de faibles taux de vitamine D avec une hausse des marqueurs de l'inflammation et de la production de derives reactifs de l'oxygene dans les echantillons de TAV et de vaisseaux et (ii) l'incubation avec de la vitamine D in vitro permettait d'attenuer le stress oxydatif dans les preparations de TAV et de vaisseaux, avec aussi une amelioration sur le plan du fonctionnement des vaisseaux. Nous rapportons ici que les taux seriques de vitamine D sont inversement proportionnels a l'ampleur du stress oxydatif dans le tissu adipeux. L'administration ex vivo de vitamine D active permettait d'attenuer le stress oxydatif lie a l'obesite. [Traduit par la Redaction] Mots-cles : tissu adipeux visceral, arteres mesenteriques, stress oxydatif, dysfonctionnement endothelial., Introduction Obesity is an age-independent, lifestyle-triggered, rapidly expanding pandemic disease (Bhupathiraju and Hu 2016) characterized by chronic systemic and adipose tissue inflammation as the major pathomechanism (Goran and Alderete 2012; [...]
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- 2020
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13. Monoamine Oxidase, Obesity and Related Comorbidities: Discovering Bonds
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Sturza, Adrian, primary, Muntean, Danina M., additional, and Crețu, Octavian M., additional
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- 2021
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14. Monoamine oxidase is a source of oxidative stress in obese patients with chronic inflammation
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Sturza, Adrian, Olariu, Sorin, Ionica, Mihaela, Duicu, Oana M., Vaduva, Adrian O., Boia, Eugen, Muntean, Danina M., and Popoiu, Calin M.
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Obesity -- Health aspects ,Adipose tissues -- Health aspects ,Mortality -- Romania ,Inflammation -- Health aspects ,Oxidative stress -- Health aspects ,Monoamine oxidase -- Health aspects ,Type 2 diabetes -- Health aspects ,Biological sciences - Abstract
Obesity is an important preventable risk factor for morbidity and mortality from cardiometabolic disease. Oxidative stress (including in visceral adipose tissue) and chronic low-grade inflammation are the major underlying pathomechanisms. Monoamine oxidase (MAO) has recently emerged as an important source of cardiovascular oxidative stress. The present study was conducted to evaluate the role of MAO as contributor to reactive oxygen species (ROS) production in white adipose tissue and vessels harvested from patients undergoing elective abdominal surgery. To this aim, visceral adipose tissue and mesenteric artery branches were isolated from obese patients with chronic inflammation and used for organ bath, ROS production, quantitative real-time PCR, and immunohistology studies. The human visceral adipose tissue and mesenteric artery branches contain mainly the MAO-A isoform, as shown by the quantitative real-time PCR and immunohistology experiments. A significant upregulation of MAO-A, the impairment in vascular reactivity, and increase in ROS production were found in obese vs. non-obese patients. Incubation of the adipose tissue samples and vascular rings with the MAO-A inhibitor (clorgyline, 30 min) improved vascular reactivity and decreased ROS generation. In conclusion, MAO-A is the predominant isoform in human abdominal adipose and vascular tissues, is overexpressed in the setting of inflammation, and contributes to the endothelial dysfunction. Key words: monoamine oxidases, obesity, inflammation, endothelial dysfunction. L'obesite est un important facteur de risque de morbidite et de mortalite liees a la maladie cardiometabolique qu'il est possible de prevenir. Le stress oxydatif (y compris dans le tissu adipeux visceral) et l'inflammation chronique de faible intensite en sont les principaux modes d'action sous-jacents. La monoamine-oxydase (MAO) est depuis peu reconnue comme etant une importante source de stress oxydatif cardiovasculaire. La presente etude a ete menee en vue d'evaluer la contribution de la MAO pour la production de derives reactifs de l'oxygene dans du tissu adipeux blanc et des vaisseaux sanguins preleves chez des patients subissant une intervention chirurgicale abdominale elective. A cette fin, nous avons isole du tissu adipeux visceral et des rameaux d'artere mesenterique chez des patients obeses presentant une inflammation chronique en vue de proceder a des etudes (i) en bain de tissu, (ii) sur la production de derives reactifs de l'oxygene, (iii) de PCR quantitatif en temps reel et (iv) d'immunohistologie. Comme l'ont montre ces deux dernieres techniques, chez l'homme, le tissu adipeux visceral et les rameaux d'artere mesenterique contiennent principalement l'isoforme MAO-A. Nous avons observe une regulation a la hausse de la MAO-A, une diminution de la reactivite vasculaire et une augmentation de la production de derives reactifs de l'oxygene plus marquer chez les patients obeses que chez les patients non obeses. L'incubation des echantillons de tissu adipeux et des anneaux vasculaires avec de la clorgyline (un inhibiteur de la MAO-A) pendant 30 minutes a permis d'ameliorer la reactivite vasculaire et de faire diminuer la production de derives reactifs de l'oxygene. En conclusion, la MAO-A est l'isoforme predominante dans les tissus adipeux et vasculaire abdominaux humains, est surexprimee en contexte d'inflammation et participe au dysfonctionnement endothelial. [Traduit par la Redaction] Mots-cles: monoamine-oxydases, obesite, inflammation, dysfonctionnement endothelial., Introduction Obesity is the most important modifiable risk factor for morbidity and mortality due to life-threatening cardiovascular diseases, type 2 diabetes, and certain cancers. With the increased adoption of the [...]
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- 2019
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15. Vitamin D improves vascular function and decreases monoamine oxidase A expression in experimental diabetes
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Sturza, Adrian, Văduva, Adrian, Uțu, Diana, Rațiu, Corina, Pop, Norbert, Duicu, Oana, Popoiu, Călin, Boia, Eugen, Matusz, Petru, Muntean, Danina M., and Olariu, Sorin
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- 2019
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16. Assessment of Platelet Mitochondrial Respiration in the Setting of Cardiopulmonary Bypass: A Case Report
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Buriman, Darius G., primary, Merce, Adrian P., additional, Bînă, Anca M., additional, Brăescu, Laurențiu A., additional, Grigorescu, Andrei E., additional, Sturza, Adrian, additional, Muntean, Danina M., additional, and Feier, Horea B., additional
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- 2023
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17. Statin-associated myopathy and the quest for biomarkers: can we effectively predict statin-associated muscle symptoms?
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Muntean, Danina M., Thompson, Paul D., Catapano, Alberico L., Stasiolek, Mariusz, Fabis, Jaroslaw, Muntner, Paul, Serban, Maria-Corina, and Banach, Maciej
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- 2017
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18. Methylene blue alleviates endothelial dysfunction and reduces oxidative stress in aortas from diabetic rats
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Privistirescu, Andreea I., Sima, Alexandra, Duicu, Oana M., Timar, Romulus, Rosca, Mariana G., Sturza, Adrian, and Muntean, Danina M.
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Aorta -- Health aspects ,Diabetes mellitus -- Physiological aspects ,Oxidative stress -- Health aspects ,Methylene blue -- Health aspects ,Biological sciences - Abstract
Endothelial dysfunction and the related increase in reactive oxygen species (ROS) production are important events in the pathophysiology of diabetes mellitus (DM). Methylene blue (MB) has been systematically investigated for its protective effects against refractory hypotension and mitochondrial dysfunction. We have previously demonstrated that MB improved mitochondrial respiration and partially decreased oxidative stress in diabetic rat hearts. The present study was aimed to investigate whether MB modulates vascular function and ROS production in thoracic aortic rings isolated from rats with streptozotocin-induced DM (after 4 weeks of hyperglycemia). The effects of MB (0.1 [micro]M, 30 min ex vivo incubation) on vascular reactivity in organ chamber (phenylephrine-induced contraction, acetylcholine-induced relaxation) and [H.sub.2][O.sub.2] production (assessed by ferrous iron xylenol orange oxidation assay) were investigated in vascular preparations with intact endothelium and after denudation. DM elicited a significant alteration of vascular function: increased contractility to phenylephrine, attenuation of acetylcholinedependent relaxation, and augmented [H.sub.2][O.sub.2] generation. Ex vivo incubation with MB partially reversed all these changes (by approximately 70%) in vascular segments with intact endothelial layer (but not in denuded vessels). In conclusion, MB might be useful in alleviating endothelial dysfunction and mitigating endothelial oxidative stress, observations that clearly require further investigation in the setting of cardiometabolic disease. Key words: methylene blue, endothelial dysfunction, oxidative stress, experimental diabetes. Le dysfonctionnement endothelial et l'augmentation de la production de derives reactifs de l'oxygene (ou ROS pour <>) qui y est liee constituent des evenements importants dans la physiopathologie du diabete sucre (DS). Le bleu de methylene (BM) a ete etudie systematiquement pour ses effets protecteurs contre l'hypotension refractaire et le dysfonctionnement mitochondrial. Nous avons montre precedemment que le BM permet d'ameliorer la respiration mitochondriale ainsi que de faire diminuer partiellement le stress oxydatif dans le creur du rat atteint de DS. Les presents travaux visaient a etudier si le BM permet de moduler la fonction vasculaire et la production de ROS dans des anneaux d'aortes thoraciques isolees de rats atteints de DS provoque par la streptozotocine (apres 4 semaines d'hyperglycemie). Nous avons etudie les effets du BM (a 0,1 [micro]M, incubation ex vivo de 30 minutes) sur la reactivite vasculaire en chambre d'organes (contraction provoquee par la phenylephrine, relaxation provoquee par l'acetylcholine) et la production de [H.sub.2][O.sub.2] (evaluee a l'aide du test d'oxydation de fer ferreux en presence de xylenol orange) dans des preparations vasculaires dont l'endothelium etait intact et apres denudation. Le DS a entraine une degradation notable de la fonction vasculaire : augmentation de la contractilite en reaction a la phenylephrine, attenuation de la relaxation dependante de l'acetylcholine et augmentation de la production d'[H.sub.2][O.sub.2]. L'incubation ex vivo avec du BM a permis d'inverser partiellement toutes ces variations (d'environ 70 %) dans les segments vasculaires dotes d'une couche endotheliale intacte (mais pas dans les vaisseaux denudes). En conclusion, le BM pourrait etre utile en vue d'attenuer le dysfonctionnement endothelial et le stress oxydatif endothelial. Ce sont des observations qui demanderaient clairement des recherches plus poussees dans un contexte de maladie cardiometabolique. [Traduit par la Redaction] Mots-cles: bleu de methylene, dysfonctionnement endothelial, stress oxydatif, diabete experimental., Introduction Diabetes mellitus (DM), a well-established independent risk factor for coronary heart disease, is currently the most serious threat to humanity health worldwide due to its alarming increase in prevalence [...]
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- 2018
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19. Cardiac Arrhythmias: Introduction, Electrophysiology of the Heart, Action Potential and Membrane Currents
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Jost, Norbert, Muntean, Danina M., Christ, Torsten, Jagadeesh, Gowraganahalli, editor, Balakumar, Pitchai, editor, and Maung-U, Khin, editor
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- 2015
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20. Methylene blue improves mitochondrial respiration and decreases oxidative stress in a substrate-dependent manner in diabetic rat hearts
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Duicu, Oana M., Privistirescu, Andreea, Wolf, Adrian, Petrus, Alexandra, Danila, Maria D., Ratiu, Corina D., Muntean, Danina M., and Sturza, Adrian
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Methylene blue -- Dosage and administration -- Patient outcomes -- Physiological aspects ,Diabetes -- Physiological aspects -- Care and treatment -- Patient outcomes ,Oxidative stress -- Care and treatment -- Patient outcomes -- Physiological aspects ,Biological sciences - Abstract
Diabetic cardiomyopathy has been systematically associated with compromised mitochondrial energetics and increased generation of reactive oxygen species (ROS) that underlie its progression to heart failure. Methylene blue is a redox drug with reported protective effects mainly on brain mitochondria. The purpose of the present study was to characterize the effects of acute administration of methylene blue on mitochondrial respiration, [H.sub.2][O.sub.2] production, and calcium sensitivity in rat heart mitochondria isolated from healthy and 2 months (streptozotocin-induced) diabetic rats. Mitochondrial respiratory function was assessed by high-resolution respirometry. [H.sub.2][O.sub.2] production and calcium retention capacity were measured spectrofluorimetrically. The addition of methylene blue (0.1 [micro]mol x [L.sup.-1]) elicited an increase in oxygen consumption of mitochondria energized with complex I and II substrates in both normal and diseased mitochondria. Interestingly, methylene blue elicited a significant increase in [H.sub.2][O.sub.2] release in the presence of complex I substrates (glutamate and malate), but had an opposite effect in mitochondria energized with complex II substrate (succinate). No changes in the calcium retention capacity of healthy or diabetic mitochondria were found in the presence of methylene blue. In conclusion, in cardiac mitochondria isolated from diabetic and nondiabetic rat hearts, methylene blue improved respiratory function and elicited a dichotomic, substrate-dependent effect on ROS production. Key words: rat heart mitochondria, diabetes mellitus, methylene blue, mitochondrial respiration, reactive oxygen species. On a systematiquement associe la cardiomyopathie diabetique a une atteinte de la fonction energetique des mitochondries et a une augmentation de la production de derives reactifs de l'oxygene (ROS), lesquels phenomenes sous-tendent son evolution vers l'insuffisance cardiaque. Le bleu de methylene est un medicament redox avec des effets protecteurs rapportes principalement dans les mitochondries cerebrales. La presente etude a ete realisee en vue de caracteriser les effets de l'administration aigue de bleu de methylene sur la respiration mitochondriale, la production de [H.sub.2][O.sub.2] et la sensibilite au calcium dans des mitochondries isolees de creurs de rats sains ou diabetiques de 2 mois (diabete provoque par la streptozotocine). Nous avons evalue la fonction respiratoire mitochondriale a l'aide de la respirometrie a haute resolution. Nous avons mesure la production de peroxyde d'hydrogene et la capacite de retention calcique a l'aide de la spectrofluorometrie. L'ajout de bleu de methylene (0,1 [micro]mol x [L.sup.-1]) a provoque une augmentation de la consommation d'oxygene par des mitochondries energisees par des substrats des complexes I et II, et ce, chez les mitochondries normales et lesees a la fois. Il est interessant de noter que le bleu de methylene a provoque une augmentation marquee de la liberation de [H.sub.2][O.sub.2] en presence de substrats du complexe I (glutamate et malate), mais qu'il avait un effet contraire dans les mitochondries energisees avec le substrat du complexe II (succinate). En presence de bleu de methylene, nous n'avons observe aucune variation de la capacite de retention du calcium dans les mitochondries saines ou diabetiques. En conclusion, dans les mitochondries isolees de creurs de rats sains ou diabetiques, le bleu de methylene permettait d'ameliorer la fonction respiratoire et provoquait un effet dichotomique et dependant du substrat sur la production de ROS. [Traduit par la Redaction] Mots-cles : mitochondrie de creur de rat, diabete sucre, bleu de methylene, respiration mitochondriale, derives reactifs de l'oxygene., Introduction Coronary heart disease is the leading cause of mortality due to myocardial infarction and of morbidity due to heart failure. In the past decades, mitochondrial dysfunction has emerged as [...]
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- 2017
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21. Contribution of monoamine oxidases to vascular oxidative stress in patients with end-stage renal disease requiring hemodialysis
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Utu, Diana, Pantea, Stelian, Duicu, Oana M., Muntean, Danina M., and Sturza, Adrian
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Chronic kidney failure -- Physiological aspects ,Oxidative stress -- Physiological aspects ,Monoamines -- Physiological aspects ,Biological sciences - Abstract
Arteriovenous fistula (AVF) is the 'lifeline' for patients with end-stage renal disease (ESRD) undergoing hemodialysis. AVF maturation failure is a poorly understood process, one of the contributors being endothelial dysfunction due to oxidative stress. Monoamine oxidases (MAOs) A and B were recently identified as novel sources of vascular oxidative stress. The aim of the present study was to assess the contribution of MAOs to the endothelial dysfunction in patients with ESDR with indication of hemodialysis. Fragments of brachial artery collaterals were harvested from ESRD patients during the surgical procedure aimed at creating the vascular access in the cubital fossa. The effect of increasing concentrations (10, 30,100 [micro]mol/L) of the irreversible MAO-A inhibitor, clorgyline, and MAO-B inhibitor, selegiline, on endothelial-dependent relaxation (EDR) in response to cumulative doses of acetylcholine was studied in isolated phenylephrine-preconstricted vascular rings. Hydrogen peroxide ([H.sub.2][O.sub.2]) production was assessed using ferrous oxidation xylenol orange assay. We showed that incubation of brachial rings with MAO inhibitors significantly improved EDR and attenuated [H.sub.2][O.sub.2] generation in patients with ESRD. MAO-related oxidative stress might contribute to the primary dysfunction/non-maturation of the AVF and MAO inhibitors could improve maturation and long-term patency of the vascular access in dialysis patients. Key words: arteriovenous fistula, monoamine oxidases, oxidative stress, endothelial dysfunction. La fistule arterioveineuse (FAV) represente la ligne de vie des patients atteints d'insuffisance renale terminale (IRT) hemodialyses. L'echec de la maturation de la FAV est un processus que l'on comprend mal, l'un des facteurs contributeurs etant le dysfonctionnement endothelial cause par le stress oxydatif. On a recemment caracterise les monoamines-oxydases (MAO) A et B comme etant de nouvelles sources de stress oxydatif vasculaire. La presente etude avait comme objectif d'evaluer la contribution des MAO dans le dysfonction endothelial chez des patients atteints d'IRT avec indication d'hemodialyse. Nous avons preleve des fragments de collaterales d'arteres brachiales de patients atteints d'IRT pendant l'intervention chirurgicale visant a creer l'acces vasculaire dans le pli du coude. Nous avons etudie l'effet de concentrations croissantes (10, 30,100 [micro]mol/L) de clorgyline, un inhibiteur irreversible de la MAO-A, et de selegiline, un inhibiteur de la MAO-B, sur la relaxation dependante de l'endothelium (RDE) en reaction a des doses cumulatives d'acetylcholine dans des anneaux vasculaires isoles precontractes par la phenylephrine. Nous avons evalue la production de peroxyde d'hydrogene ([H.sub.2][O.sub.2]) a l'aide de l'epreuve d'oxydation ferreuse avec l'orange de xylenol. Nous avons montre que l'incubation d'anneaux brachiaux avec des inhibiteurs de la MAO permettait nettement d'ameliorer la RDE et d'attenuer la production d'[H.sub.2][O.sub.2] chez les patients atteints d'IRT. Le stress oxydatif lie aux MAO pourrait contribuer au dysfonctionnement ou a la non-maturation primaires de la FAV, et les inhibiteurs de la MAO pourraient permettre d'ameliorer la maturation et la permeabilite a long terme de l'acces vasculaire chez les patients dialyses. [Traduit par la Redaction] Mots-cles: fistule arterioveineuse, monoamines-oxydases, stress oxydatif, dysfonctionnement endothelial., Introduction Chronic kidney disease (CKD) is a characterized by an irreversible alteration of renal structure and function, lasting more than 3 months, and the association with a plethora of complications: [...]
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- 2017
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22. Untargeted Metabolomics by Ultra-High-Performance Liquid Chromatography Coupled with Electrospray Ionization-Quadrupole-Time of Flight-Mass Spectrometry Analysis Identifies a Specific Metabolomic Profile in Patients with Early Chronic Kidney Disease
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Glavan, Mihaela-Roxana, primary, Socaciu, Carmen, additional, Socaciu, Andreea Iulia, additional, Gadalean, Florica, additional, Cretu, Octavian M., additional, Vlad, Adrian, additional, Muntean, Danina M., additional, Bob, Flaviu, additional, Milas, Oana, additional, Suteanu, Anca, additional, Jianu, Dragos Catalin, additional, Stefan, Maria, additional, Balint, Lavinia, additional, Ienciu, Silvia, additional, and Petrica, Ligia, additional
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- 2023
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23. Stimulation of P2Y11 receptor protects human cardiomyocytes against Hypoxia/Reoxygenation injury and involves PKCε signaling pathway
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Benoist, Lauriane, Chadet, Stéphanie, Genet, Thibaud, Lefort, Claudie, Heraud, Audrey, Danila, Maria D., Muntean, Danina M., Baron, Christophe, Angoulvant, Denis, Babuty, Dominique, Bourguignon, Thierry, and Ivanes, Fabrice
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- 2019
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24. Metformin and empagliflozin modulate monoamine oxidase-related oxidative stress and improve vascular function in human mammary arteries
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Lascu, Ana, primary, Ionică, Loredana N., additional, Buriman, Darius G., additional, Merce, Adrian P., additional, Deaconu, Loredana, additional, Borza, Claudia, additional, Crețu, Octavian M., additional, Sturza, Adrian, additional, Muntean, Danina M., additional, and Feier, Horea B., additional
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- 2022
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25. Mitochondrial Effects of Common Cardiovascular Medications: The Good, the Bad and the Mixed
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Bețiu, Alina M., primary, Noveanu, Lavinia, additional, Hâncu, Iasmina M., additional, Lascu, Ana, additional, Petrescu, Lucian, additional, Maack, Christoph, additional, Elmér, Eskil, additional, and Muntean, Danina M., additional
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- 2022
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26. The effect of purinergic signaling via the P2Y11 receptor on vascular function in a rat model of acute inflammation
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Dănilă, Maria D., Privistirescu, Andreea, Duicu, Oana M., Rațiu, Corina D., Angoulvant, Denis, Muntean, Danina M., and Sturza, Adrian
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- 2017
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27. Metformin Reverses the Effects of Angiotensin 2 in Human Mammary Arteries by Modulating the Expression of Nitric Oxide Synthases
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Merce, Adrian, primary, Buriman, Darius G., additional, Lascu, Ana, additional, Bînă, Anca M., additional, Feier, Horea B., additional, Petrescu, Lucian, additional, Borza, Claudia, additional, Sturza, Adrian, additional, Muntean, Danina M., additional, and Crețu, Octavian M., additional
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- 2022
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28. Cell-Permeable Succinate Improves Platelet Respiration in Patients Undergoing Cardiopulmonary Bypass: A Pilot Study
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Merce, Adrian P., primary, Bînă, Anca M., additional, Avram, Vlad F., additional, Buriman, Darius G., additional, Lascu, Ana, additional, Feier, Horea B., additional, Petrescu, Lucian, additional, Muntean, Danina M., additional, Elmér, Eskil, additional, and Crețu, Octavian M., additional
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- 2022
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29. Monoamine oxidase is a source of cardiac oxidative stress in obese rats: the beneficial role of metformin
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Merce, Adrian P., primary, Ionică, Loredana N., additional, Bînă, Anca M., additional, Popescu, Simona, additional, Lighezan, Rodica, additional, Petrescu, Lucian, additional, Borza, Claudia, additional, Sturza, Adrian, additional, Muntean, Danina M., additional, and Creţu, Octavian M., additional
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- 2022
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30. Acute inhibition of monoamine oxidase and ischemic preconditioning in isolated rat hearts: interference with postischemic functional recovery but no effect on infarct size reduction
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Danila, Maria D., Privistirescu, Andreea I., Mirica, Silvia N., Sturza, Adrian, Ordodi, Valentin, Noveanu, Lavinia, Duicu, Oana M., and Muntean, Danina M.
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Heart diseases -- Development and progression -- Care and treatment ,Enzymes -- Regulation ,Monoamine oxidase -- Health aspects ,Biological sciences - Abstract
Monoamine oxidases (MAOs) have recently emerged as important mitochondrial sources of oxidative stress in the cardiovascular system. Generation of reactive oxygen species during the brief episodes of ischemic preconditioning (IPC) is responsible for the cardioprotection at reperfusion. The aim of this study was to assess the effects of two MAO inhibitors (clorgyline and pargyline) on the IPC-related protection in isolated rat hearts. Animals subjected to 30 min global ischemia and 120 min reperfusion were assigned to the following groups: (i) Control, no additional intervention; (ii) IPC, 3 cycles of 5 min ischemia and 5 min reperfusion before the index ischemia; (iii) IPC-clorgyline, IPC protocol bracketed for 5 min with clorgyline (50 µmol/L); (iv) IPC-pargyline, IPC protocol bracketed for 5 min with pargyline (0.5 mmol/L). The postischemic functional recovery was assessed by the left ventricular developed pressure (LVDP) and the indices of contractility (+dLVP/dt max) and relaxation (-dLVP/dt max). Infarct size (IS) was quantified by TTC staining. In both genders, IPC significantly improved functional recovery that was further enhanced in the presence of either clorgyline or pargyline. IS reduction was comparable among all the preconditioned groups, regardless of the presence of MAO inhibitors. In isolated rat hearts, acute inhibition of MAOs potentiates the IPC-induced postischemic functional recovery without interfering with the anti-necrotic protection. Key words: monoamine oxidase, MAO inhibitors, ischemic preconditioning, isolated rat heart. Les monoamine oxydases (MAOs) se sont recemment revelees d'importantes sources de stress oxydatif mitochondrial dans le systeme cardiovasculaire. La generation de derives reactifs de l'oxygene au cours d'episodes brefs de preconditionnement ischemique (PCI) est responsable de la cardioprotection lors de la reperfusion. La presente etude visait a evaluer les effets de deux inhibiteurs de la MAO (la clorgyline et la pargyline) sur le PCI dans un modele de caeur isole de rat. Nous avons soumis les animaux a une ischemie globale de 30 min, puis a une reperfusion de 120 min et les avons repartis dans les groupes suivants: (i) temoin (aucune intervention supplementaire), (ii) PCI (3 cycles de 5 min d'ischemie suivis de 5 min de reperfusion avant l'ischemie de reference), (iii) PCI-clorgyline (protocole de PCI alternant avec l'administration de clorgyline a 50 µmol/L pendant 5 min) et (iv) PCI-pargyline (protocole de PCI alternant avec l'administration de pargyline a 0,5 mmol/L pendant 5 min). Nous avons ensuite evalue le retablissement fonctionnel post-ischemique en mesurant la pression ventriculaire gauche developpee (PVGD) ainsi que les indices de contractilite (+dP/dt max) et de relaxation (-dP/dt max). Enfin, nous avons quantifie la taille de l'infarctus par la technique de coloration au TTC. Chez les animaux des deux sexes, le PCI a permis d'ameliorer clairement le retablissement fonctionnel qui a ete accentue en presence de clorgyline ou de pargyline. Par ailleurs, la diminution de la taille de l'infarctus etait comparable dans tous les groupes soumis au preconditionnement, et ce, sans egard a la presence d'inhibiteurs de la MAO. En somme, dans les caeurs isoles de rat, l'administration a court terme d'inhibiteurs de la MAO potentialise la recuperation fonctionnelle post-ischemique induite par le PCI, sans nuire a la protection contre la necrose. [Traduit par la Redaction] Mots-cles: monoamine-oxydase, inhibiteurs de la MAO, preconditionnement ischemique, caeur isole de rat., Introduction Coronary heart disease remains the leading cause of mortality and morbidity due to heart failure worldwide (Go et al. 2014). In the past decades, mitochondria have emerged as key [...]
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- 2015
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31. Modulation of mitochondrial respiratory function and ROS production by novel benzopyran analogues
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Petrus, Alexandra, Duicu, Oana M., Sturza, Adrian, Noveanu, Lavinia, Kiss, Lorand, Danila, Maria, Baczko, Istvan, Muntean, Danina M., and Jost, Norbert
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Drugs -- Structure-activity relationships ,Polycyclic compounds -- Properties ,Structure-activity relationship (Pharmacology) -- Observations ,Pharmacology, Experimental ,Reactive oxygen species -- Properties ,Dose-response relationship (Biochemistry) -- Research ,Biological sciences - Abstract
A substantial body of evidence indicates that pharmacological activation of mitochondrial ATP-sensitive potassium channels (m[K.sub.ATP]) in the heart is protective in conditions associated with ischemia/reperfusion injury. Several mechanisms have been postulated to be responsible for cardioprotection, including the modulation of mitochondrial respiratory function. The aim of the present study was to characterize the dose-dependent effects of novel synthetic benzopyran analogues, derived from a BMS-191095, a selective m[K.sub.ATP] opener, on mitochondrial respiration and reactive oxygen species (ROS) production in isolated rat heart mitochondria. Mitochondrial respiratory function was assessed by high-resolution respirometry, and [H.sub.2][O.sub.2] production was measured by the Amplex Red fluorescence assay. Four compounds, namely KL-1487, KL-1492, KL-1495, and KL-1507, applied in increasing concentrations (50, 75, 100, and 150 µmol/L, respectively) were investigated. When added in the last two concentrations, all compounds significantly increased State 2 and 4 respiratory rates, an effect that was not abolished by 5-hydroxydecanoate (5-HD, 100 µmol/L), the classic m[K.sub.ATP] inhibitor. The highest concentration also elicited an important decrease of the oxidative phosphorylation in a [K.sup.+] independent manner. Both concentrations of 100 and 150 µmol/L for KL-1487, KL-1492, and KL-1495, and the concentration of 150 µmol/L for KL-1507, respectively, mitigated the mitochondrial [H.sub.2][O.sub.2] release. In isolated rat heart mitochondria, the novel benzopyran analogues act as protonophoric uncouplers of oxidative phosphorylation and decrease the generation of reactive oxygen species in a dose-dependent manner. Key words: rat heart mitochondria, benzopyran analogues, protonophores, uncoupling, hydrogen peroxide. De plus en plus de donnees indiquent que l'activation pharmacologique des canaux potassiques sensibles a l'ATP de la mitochondrie (m[K.sub.ATP]) du coeur le protege lorsqu'il est expose a des conditions associees au dommage d'ischemie/reperfusion. Plusieurs mecanismes pourraient etre responsables de la cardioprotection incluant la modulation de la fonction respiratoire mitochondriale. Le but de l'etude presente etait de caracteriser les effets lies a la dose de nouveaux analogues synthetiques du benzopyrane, derives du BMS-191095, un compose qui ouvre selectivement les m[K.sub.ATP], sur la respiration mitochondriale et la production d'especes reactives d'oxygene (ERO) dans les mitochondries isolees du coeur de rat et ce. La fonction respiratoire mitochondriale a ete evaluee par respirometrie a haute resolution et la production de [H.sub.2][O.sub.2] a ete mesuree par un dosage en fluorescence a l'aide de la trousse Amplex Red. Quatre composes, a savoir KL-1487, KL-1492, KL-1495 et KL-1507, ajoutes en concentrations croissantes (50,75,100 et 150 µmol/L, respectivement), ont ete examines. Lorsqu'ajoutes aux deux concentrations les plus elevees, tous les composes accroissaient significativement les taux respiratoires aux etats 2 et 4, effet qui n'etait pas aboli par le 5-hydroxydecanoate (5-HD, 100 µmol/L), l'inhibiteur classique des m[K.sub.ATP]. La plus forte concentration induisait aussi une diminution importante de la phosphorylation oxydative de maniere independante du [K.sup.+]. Les deux concentrations de 100 µmol/L et 150 µmol/L de KL-1487, KL-1492 et KL-1495, et la concentration de 150 µmol/L de KL-1507 diminuaient respectivement la liberation de [H.sub.2][O.sub.2] de la mitochondrie. Les nouveaux analogues du benzopyrane agissent comme decouplants protonophores de la phosphorylation oxydative dans les mitochondries isolees du coeur de rat, et diminuent la generation d'especes reactives d'oxygene en fonction de leur concentration. [Traduit par la Redaction] Mots-cles : mitochondries du coeur de rat, analogues du benzopyrane, protonophores, effet decouplant, peroxyde d'hydrogene., Introduction In the past decades mitochondria have emerged as major contributors to the pathogenesis of myocardial ischemia/reperfusion (I/R) injury as well as important therapeutic targets in cardioprotection (Camara et al. [...]
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- 2015
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32. Monoamine oxidases are novel sources of cardiovascular oxidative stress in experimental diabetes
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Sturza, Adrian, Duicu, Oana M., Vaduva, Adrian, Danila, Maria D., Noveanu, Lavinia, Varro, Andras, and Muntean, Danina M.
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Diabetes -- Physiological aspects ,Oxidases -- Health aspects ,Oxidative stress -- Health aspects ,Biological sciences - Abstract
Diabetes mellitus (DM) is widely recognized as the most severe metabolic disease associated with increased cardiovascular morbidity and mortality. The generation of reactive oxygen species (ROS) is a major event causally linked to the development of cardiovascular complications throughout the evolution of DM. Recently, monoamine oxidases (MAOs) at the outer mitochondrial membrane, with 2 isoforms, MAO-A and MAO-B, have emerged as novel sources of constant hydrogen peroxide ([H.sub.2][O.sub.2]) production in the cardiovascular system via the oxidative deamination of biogenic amines and neurotransmitters. Whether MAOs are mediators of endothelial dysfunction in DM is unknown, and so we studied this in a streptozotocin-induced rat model of diabetes. MAO expression (mRNA and protein) was increased in both arterial samples and hearts isolated from the diabetic animals. Also, [H.sub.2][O.sub.2] production (ferrous oxidation--xylenol orange assay) in aortic samples was significantly increased, together with an impairment of endothelium-dependent relaxation (organ-bath studies). MAO inhibitors (clorgyline and selegiline) attenuated ROS production by 50% and partially normalized the endothelium-dependent relaxation in diseased vessels. In conclusion, MAOs, in particular the MAO-B isoform, are induced in aortas and hearts in the streptozotocin-induced diabetic rat model and contribute, via the generation of [H.sub.2][O.sub.2], to the endothelial dysfunction associated with experimental diabetes. Key words: monoamine oxidases, experimental diabetes mellitus, oxidative stress, endothelial dysfunction, clorgyline, selegiline. Il est largement accepte que le diabete sucre est la maladie metabolique la plus grave, associee a une morbidite et une mortalite cardiovasculares. La production de derives reactifs de l'oxygene (DRO) est une manifestation majeure entrainant des complications cardiovasculaires tout au long de la progression du diabete sucre. Recemment, les monoamine oxydases (MAO) de la membrane mitochondriale externe sous deux isoformes (MAO-A et MAO-B) se sont demarquees comme de nouvelles sources de production constante de peroxyde d'hydrogene ([H.sub.2][O.sub.2]) dans le systeme cardiovasculaire par l'intermediaire de la desamination oxydative des amines biogenes et des neurotransmetteurs. On ne sait pas si les MAO sont des mediateurs de la dysfonction endotheliale dans le diabete sucre, et c'est ce que nous avons etudie avec ce modele de diabete induit par la streptozotocine chez le rat. L'expression des MAO (ARNm et proteines) augmentait dans les echantillons arteriels comme dans les creurs isoles d'animaux diabetiques. De plus, la production de [H.sub.2][O.sub.2] (test de l'oxydation des ions ferreux revelee par le xylenol orange) dans des echantillons d'aorte etait nettement accrue et associee a un deficit de la relaxation dependante de l'endothelium (etudes en bain d'organe). L'administration des inhibiteurs des MAO (clorgyline et selegiline) a permis de diminuer la production de DRO de 50% et est parvenue en partie a retablir la relaxation dependante de l'endothelium a une valeur normale dans les vaisseaux atteints. En conclusion, dans le modele de diabete induit par la streptozotocine chez le rat, les MAO, en particulier l'isoforme MAO-B, sont induites dans les aortes et les creurs des animaux et contribuent par la production de [H.sub.2][O.sub.2] a la dysfonction endotheliale observee dans un modele experimental du diabete. [Traduit par la Redaction] Mots-cles: monoamine oxydases, diabete sucre experimental, stress oxydatif, dysfonction endotheliale, clorgyline, selegiline., Introduction Diabetes mellitus (DM), the most severe metabolic disease associated with increased cardiovascular morbidity and mortality, is widely recognized nowadays as a serious threat to global health, owing to its [...]
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- 2015
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33. Assessment of the Systemic Oxidative Stress in Preeclampsia
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Bînă, Anca M., primary, Anechitei, Andreea I., additional, Lelcu, Theia, additional, Lința, Adina V., additional, Chiriac, Daniela V., additional, Mocanu, Adelina G., additional, Bernad, Elena, additional, Popa, Zoran L., additional, Craina, Marius L., additional, Muntean, Danina M., additional, Borza, Claudia, additional, and Crețu, Octavian M., additional
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- 2022
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34. Assessment of Platelet Mitochondrial Respiration in a Pediatric Population: A Pilot Study in Healthy Children and Children with Acute Lymphoblastic Leukemia
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Lelcu, Theia, primary, Bînă, Anca M., additional, Dănilă, Maria D., additional, Popoiu, Călin M., additional, Aburel, Oana M., additional, Arghirescu, Smaranda T., additional, Borza, Claudia, additional, and Muntean, Danina M., additional
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- 2021
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35. Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Amiodarone Toxicity
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Bețiu, Alina M., Chamkha, Imen, Gustafsson, Ellen, Meijer, Elna, Avram, Vlad F., Frostner, Eleonor Åsander, Ehinger, Johannes K., Petrescu, Lucian, Muntean, Danina M., and Elmér, Eskil
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Blood Platelets ,QH301-705.5 ,NV118 ,Cell Respiration ,Succinic Acid ,Amiodarone ,Hep G2 Cells ,Protective Agents ,Article ,sotalol ,Mitochondria ,ATP ,desethylamiodarone ,Chemistry ,Adenosine Triphosphate ,platelets ,PBMCs ,Humans ,Prodrugs ,Biology (General) ,HepG2 cells ,QD1-999 ,Anti-Arrhythmia Agents ,respiration - Abstract
Amiodarone is a potent antiarrhythmic drug and displays substantial liver toxicity in humans. It has previously been demonstrated that amiodarone and its metabolite (desethylamiodarone, DEA) can inhibit mitochondrial function, particularly complexes I (CI) and II (CII) of the electron transport system in various animal tissues and cell types. The present study, performed in human peripheral blood cells, and one liver-derived human cell line, is primarily aimed at assessing the concentration-dependent effects of these drugs on mitochondrial function (respiration and cellular ATP levels). Furthermore, we explore the efficacy of a novel cell-permeable succinate prodrug in alleviating the drug-induced acute mitochondrial dysfunction. Amiodarone and DEA elicit a concentration-dependent impairment of mitochondrial respiration in both intact and permeabilized platelets via the inhibition of both CI- and CII-supported respiration. The inhibitory effect seen in human platelets is also confirmed in mononuclear cells (PBMCs) and HepG2 cells. Additionally, amiodarone elicits a severe concentration-dependent ATP depletion in PBMCs, which cannot be explained solely by mitochondrial inhibition. The succinate prodrug NV118 alleviates the respiratory deficit in platelets and HepG2 cells acutely exposed to amiodarone. In conclusion, amiodarone severely inhibits metabolism in primary human mitochondria, which can be counteracted by increasing mitochondrial function using intracellular delivery of succinate.
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- 2021
36. Mitochondrial physiology: Gnaiger Erich et al ― MitoEAGLE Task Group
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Gnaiger, Erich, Aasander Frostner, Eleonor, Abdul Karim, Norwahidah, Abdel-Rahman, Engy Ali, Abumrad, Nada A, Acuna-Castroviejo, Dario, Adiele, Reginald C, Ahn, Bumsoo, Alencar, MB, Ali, Sameh S, Almeida, Angeles, Alton, Lesley, Alves, Marco G, Amati, Francesca, Amoedo, Nivea Dias, Amorim, Ricardo, Anderson, Ethan J, Andreadou, Ioanna, Antunes, Diana, Arago, Marc, Aral, Cenk, Arandarcikaite, Odeta, Arias-Reyes, Christian, Armand, Anne-Sophie, Arnould, Thierry, Avram, Vlad Florian, Axelrod, Christopher L, Bairam, Aida, Bailey, Damian M, Bajpeyi, Sudip, Bajzikova, Martina, Bakker, Barbara M, Barlow, Jonathan, Bardal, Tora, Banni, A, Bastos Sant'Anna Silva, Ana Carolina, Batterson, Philip, Battino, Maurizio, Bazil, Jason, Beard, Daniel A, Beleza, Jorge, Bednarczyk, Piotr, Bello, Fiona, Ben-Shachar, Dorit, Bento Guida, Jose Freitas, Bergdahl, Andreas, Berge, Rolf K, Bergmeister, Lisa, Bernardi, Paolo, Berridge, Michael V, Bettinazzi, Stefano, Bishop, David, Blier, Pierre U, Blindheim, Dan Filip, Boardman, Neoma T, Boetker, Hans Erik, Borchard, Sabine, Boros, Mihaly, Borsheim, Elisabet, Borras, Consuelo, Borutaite, Vilma, Botella, Javier, Bouillaud, Frederic, Bouitbir, Jamal, Boushel, Robert C, Bovard, Josh, Bravo-Sagua, Roberto, Breton, Sophie, Brown, David A, Brown, Guy C, Brown, Robert A, Brozinick, Joseph T, Buettner, Garry R, Burtscher, Johannes, Bustos, Matilde, Calabria, Elisa, Calbet, Jose A, Calzia, Enrico, Cannon, Daniel T, Cano Sanchez, Maria, Canto Alvarez, Carles, Cardinale, D, Cardoso, Luiza Helena Daltro, Carvalho, Eugenia, Casado Pinna, Marta, Cassar, Samantha, Castelo, Maria P, Castilho, Roger F, Cavalcanti-de-Albuquerque, Joao Paulo, Cecatto, Cristiane, Celen, Murat C, Cervinkova, Zuzana, Chabi, Beatrice, Chakrabarti, Lisa, Chakrabarti, Sasanka, Chaurasia, Bhagirath, Chen, Quan, Chicco, Adam J, Chinopoulos, Christos, Chowdhury, Subir K, Cizmarova, Beata, Clementi, Emilio, Coen, Paul M, Cohen, Bruce H, Coker, Robert H, Collin-Chenot, Anne, Coughlan, Melinda T, Coxito, Petro, Crisostomo, Luis, Crispim, Marcell, Crossland, Hannah, Dahdah, Norma, Dalgaard, Louise T, Dambrova, Maija, Danhelovska, Tereza, Darveau, Charles A, Darwin, Paula M, Das, Anibh M, Dash, Ranjan K, Davidova, Eliska, Davis, Michael S, Dayanidhi, Sudarshan, De Bem, Andreza Fabro, De Goede, Paul, De Palma, Clara, De Pinto, Vito, Dela, F, Dembinska-Kiec, Aldona, Detraux, Damien, Devaux, Yvan, Di Marcello, Marco, Di Paola, Floriana Jessica, Dias, Candida, Dias, Tania R, Diederich, Marc, Distefano, Giovanna, Djafarzadeh, Siamak, Doermann, Niklas, Doerrier, Carolina, Dong, Lan-Feng, Donnelly, Chris, Drahota, Zdenek, Duarte, Filipe Valente, Dubouchaud, Herve, Duchen, Michael R, Dumas, Jean-Francois, Durham, William J, Dymkowska, Dorota, Dyrstad, Sissel E, Dyson, Alex, Dzialowski, Edward M, Eaton, Simon, Ehinger, Johannes, Elmer, Eskil, Endlicher, Rene, Engin, Ayse B, Escames, Germaine, Evinova, Andrea, Ezrova, Zuzana, Falk, Marni Joy, Fell, David A, Ferdinandy, Peter, Ferko, Miroslav, Fernandez-Ortiz, Marisol, Erika, Fernandez-Vizarra, Ferreira, Julio Cesar Batista, Ferreira, Rita, Ferri, Alessandra, Festuccia, WT, Fessel, Joshua P, Filipovska, Aleksandra, Fisar, Zdenek, Fischer, Christine, Fischer, Michael, Fisher, Gordon, Fisher, Joshua J, Fontanesi, Flavia, Forbes-Hernandez, Tamara Y, Ford, Ellen, Fornaro, Mara, Fuertes Agudo, Marina, Fulton, Montana, Galina, Antonio, Galkin, Alexander, Gallee, Leon, Galli, Gina L, Gama Perez, Pau, Gan, Zhenji, Ganetzky, Rebecca, Gao, Yun, Garcia, Geovana S, Garcia-Rivas, Gerardo, Garcia-Roves, Pablo Miguel, Garcia-Souza, Luiz Felipe, Garlid, Keith D, Garrabou, Gloria, Garten, Antje, Gastaldelli, Amalia, Gayen, Jiaur, Genders, Amanda J, Genova, Maria Luisa, Giampieri, Francesca, Glatz, Jan FC, Giovarelli, Matteo, Goikoetxea Usandizaga, Naroa, Goncalo Teixeira da Silva, Rui, Goncalves, Debora Farina, Gonzalez-Armenta, Jenny L, Gonzalez-Francesqua, A, Gonzalez-Freire, Marta, Gonzalo, Hugo, Goodpaster, Bret H, Gorr, Thomas A, Gourlay, Campbell W, Grams, Bente, Granata, Cesare, Grefte, Sander, Grilo, Luis, Guarch, Meritxell Espino, Gueguen, Naig, Gumeni, Sentiljana, Haas, Clarissa B, Haavik, Jan, Hachmo, Yafit, Haendeler, Judith, Haider, Markus, Hajrulahovic, Anesa, Hamann, Andrea, Han, Jin, Han, Woo Hyun, Hancock, Chad R, Hand, Steven C, Handl, Jiri, Hansikova, Hana, Hardee, Justin P, Hargreaves, Ian P, Harper, Mary Ellen, Harrison, David K, Hassan, Hazirah, Hatakova, Zuzana, Hausenloy, Derek J, Heales, Simon JR, Heiestad, Christina, Hellgren, Kim T, Henrique, Alexandrino, Hepple, Russell T, Hernansanz-Agustin, Pablo, Hewakapuge, Sudinna, Hickey, Anthony J, Ho, Dieu Hien, Hoehn, Kyle L, Hoel, Frederik, Holland, Olivia J, Holloway, Graham P, Holzner, Lorenz, Hoppel, Charles L, Hoppeler, H, Hoppel, Florian, Houstek, Josef, Huete-Ortega, Maria, Hyrossova, Petra, Iglesias-Gonzalez, Javier, Indiveri, Cesare, Irving, Brian A, Isola, Raffaella, Iyer, Shilpa, Jackson, Christophe B, Jadiya, Pooja, Jana, Prado Fabian, Jandeleit-Dahm, K, Jang, David H, Jang, Young C, Janowska, Joanna, Jansen, Kirsten, Jansen-Duerr, Pidder, Jansone, Baiba, Jarmuszkiewicz, Wieslawa, Jaskiewicz, Anna, Jaspers, Richard T, Jedlicka, Jan, Jerome, Estaquier, Jespersen, Nichlas R, Jha, Rajan K, Joseph, Vincent, Juhasz, Laszlo, Jurczak, Michael J, Jurk, Diana, Kaambre, Tuuli, Kaczor, Jan J, Kainulainen, Heikki, Kampa, Rafal Pawel, Kandel, Sunil M, Kane, Daniel A, Kapferer, Werner, Kapnick, Senta, Kappler, Lisa, Karabatsiakis, Alexander, Karavaeva, Iuliia, Karkucinska-Wieckowska, Agnieszka, Kaur, Sarbjot, Keijer, Jaap, Keller, Markus A, Keppner, Gloria, Khamoui, Andy V, Kidere, Dita, Kilbaugh, Todd, Kim, Hyoung Kyu, Kim, Julian KS, Kimoloi, Sammy, Klepinin, Aleksandr, Klepinina, Lyudmila, Klingenspor, Martin, Klocker, Helmut, Komlódi, Timea, Kolasa, Iris, Koopman, Werner JH, Kopitar-Jerala, Natasa, Kowaltowski, Alicia J, Kozlov, Andrey V, Krajcova, Adela, Krako Jakovljevic, Nina, Kristal, Bruce S, Krycer, Jamer 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GG, McStay, Gavin P, Menze, Michael A, Mendham, Amy, Mercer, John R, Merz, Tamara, Messina, Angela, Meszaros, Andras T, Methner, Axel, Michalak, Slawomir, Mila Guasch, Maria, Minuzzi, Luciele M, Misirkic Marjanovic, Maja, Moellering, Douglas R, Moisoi, Nicoleta, Molina, Anthony JA, Montaigne, David, Moore, Anthony L, Moore, Christy, Moreau, Kerrie, Moreira, Bruno P, Moreno-Sanchez, Rafael, Mracek, Tomas, Muccini, Anna Maria, Muntane, Jordi, Muntean, Danina M, Murray, Andrew J, Musiol, Eva, Nabben, Miranda, Nair, K Sreekumaran, Nehlin, Jan O, Nemec, Michal, Nesci, Salvatore, Neufer, P Darrell, Neuzil, Jiri, Neviere, Remi, Newsom, Sean A., Norman, Jennifer, Nozickova, Katerina, Nunes, Sara, Nuoffer, Jean-Marc, O'Brien, Kristin, O'Brien, Katie A, O'Gorman, Donal, Olgar, Yusuf, Oliveira, Ben, Oliveira, Jorge, Oliveira, Marcus F, Oliveira, Marcos Tulio, Oliveira, Pedro F, Oliveira, Paulo J, Olsen, Rolf Erik, Orynbayeva, Zulfiya, Osiewacz, Heinz D, Paez, Hector, Pak, Youngmi K, Pallotta, 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Zikova, Alena, Zischka, Hans, Zorzano, Antonio, Zujovic, Tijana, Zurmanova, Jitka, Zvejniece, Liga, Lagarrigue, Sylviane, Munro, Daniel, Pereira, Susana, Laranjinha, Joäo, Hecker, Matthias, Jusic, Amela, Prigione, Alessandro, Sommer, Natascha, Weissig, Volkmar, Guida, Bento, G, John G, Jones, JG, AMS - Tissue Function & Regeneration, AMS - Rehabilitation & Development, Physiology, Mito-Eagle - Evolution-Age-Gender-Lifestyle-Environment (Mito-Eagle), Oroboros Instruments, Dynamique Musculaire et Métabolisme (DMEM), Université de Montpellier (UM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), and Gnaiger Erich, Aasander Frostner Eleonor, Abdul Karim Norwahidah, Abdel-Rahman Engy Ali, Abumrad Nada A, Acuna-Castroviejo Dario, Adiele Reginald C, Ahn Bumsoo, Alencar Mayke Bezerra, Ali Sameh S, Almeida Angeles, Alton Lesley, Alves Marco G, Amati Francesca, Amoedo Nivea Dias, Amorim Ricardo, Anderson Ethan J, Andreadou Ioanna, Antunes Diana, Arago Marc, Aral Cenk, Arandarcikaite Odeta, Arias-Reyes Christian, Armand Anne-Sophie, Arnould Thierry, Avram Vlad F, Axelrod Christopher L, Bailey Damian M, Bairam Aida, Bajpeyi Sudip, Bajzikova Martina, Bakker Barbara M, Banni Aml, Bardal Tora, Barlow J, Bastos Sant'Anna Silva Ana Carolina, Batterson Philip M, Battino Maurizio, Bazil Jason N, Beard Daniel A, Bednarczyk Piotr, Beleza Jorge, Bello Fiona, Ben-Shachar Dorit, Bento Guida Jose Freitas, Bergdahl Andreas, Berge Rolf K, Bergmeister Lisa, Bernardi Paolo, Berridge Michael V, Bettinazzi Stefano, Bishop David J, Blier Pierre U, Blindheim Dan Filip, Boardman Neoma T, Boetker Hans Erik, Borchard Sabine, Boros Mihaly, Boersheim Elisabet, Borras Consuelo, Borutaite Vilma, Botella Javier, Bouillaud Frederic, Bouitbir Jamal, Boushel Robert C, Bovard Josh, Bravo-Sagua Roberto, Breton Sophie, Brown David A, Brown Guy C, Brown Robert Andrew, Brozinick Joseph T, Buettner Garry R, Burtscher Johannes, Bustos Matilde, Calabria Elisa, Calbet Jose 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Gama Perez Pau, Gan Zhenji, Ganetzky Rebecca, Gao Yun, Garcia Geovana S, Garcia-Rivas Gerardo, Garcia-Roves Pablo Miguel, Garcia-Souza Luiz F, Garlid Keith D, Garrabou Gloria, Garten Antje, Gastaldelli Amalia, Gayen Jiaur, Genders Amanda J, Genova Maria Luisa, Giampieri Francesca, Giovarelli Matteo, Glatz Jan FC, Goikoetxea Usandizaga Naroa, Goncalo Teixeira da Silva Rui, Goncalves Debora Farina, Gonzalez- Armenta Jenny L, Gonzalez-Franquesa Alba, Gonzalez-Freire Marta, Gonzalo Hugo, Goodpaster Bret H, Gorr Thomas A, Gourlay Campbell W, Grams Bente, Granata Cesare, Grefte Sander, Grilo Luis, Guarch Meritxell Espino, Gueguen Naig, Gumeni Sentiljana, Haas Clarissa, Haavik Jan, Hachmo Yafit, Haendeler Judith, Haider Markus, Hajrulahovic Anesa, Hamann Andrea, Han Jin, Han Woo Hyun, Hancock Chad R, Hand Steven C, Handl Jiri, Hansikova Hana, Hardee Justin P, Hargreaves Iain P, Harper Mary- Ellen, Harrison David K, Hassan Hazirah, Hatokova Zuzana, Hausenloy Derek J, Heales Simon JR, Hecker Matthias, Heiestad Christina, Hellgren Kim T, Henrique Alexandrino, Hepple Russell T, Hernansanz- Agustin Pablo, Hewakapuge Sudinna, Hickey Anthony J, Ho Dieu Hien, Hoehn Kyle L, Hoel Fredrik, Holland Olivia J, Holloway Graham P, Holzner Lorenz, Hoppel Charles L, Hoppel Florian, Hoppeler Hans, Houstek Josef, Huete-Ortega Maria, Hyrossova Petra, Iglesias-Gonzalez Javier, Indiveri Cesare, Irving Brian A, Isola Raffaella, Iyer Shilpa, Jackson Christopher Benjamin, Jadiya Pooja, Jana Prado Fabian, Jandeleit-Dahm Karin, Jang David H, Jang Young Charles, Janowska Joanna, Jansen Kirsten M, Jansen-Duerr Pidder, Jansone Baiba, Jarmuszkiewicz Wieslawa, Jaskiewicz Anna, Jaspers Richard T, Jedlicka Jan, Jerome Estaquier, Jespersen Nichlas Riise, Jha Rajan Kumar, Jones John G, Joseph Vincent, Juhasz Laszlo, Jurczak Michael J, Jurk Diana, Jusic Amela, Kaambre Tuuli, Kaczor Jan Jacek, Kainulainen Heikki, Kampa Rafal Pawel, Kandel Sunil Mani, Kane Daniel A, Kapferer Werner, Kapnick Senta, Kappler Lisa, Karabatsiakis Alexander, Karavaeva Iuliia, Karkucinska-Wieckowska Agnieszka, Kaur Sarbjot, Keijer Jaap, Keller Markus A, Keppner Gloria, Khamoui Andy V, Kidere Dita, Kilbaugh Todd, Kim Hyoung Kyu, Kim Julian KS, Kimoloi Sammy, Klepinin Aleksandr, Klepinina Lyudmila, Klingenspor Martin, Klocker Helmut, Kolassa Iris, Komlodi Timea, Koopman Werner JH, Kopitar-Jerala Natasa, Kowaltowski Alicia J, Kozlov Andrey V, Krajcova Adela, Krako Jakovljevic Nina, Kristal Bruce S, Krycer James R, Kuang Jujiao, Kucera Otto, Kuka Janis, Kwak Hyo Bum, Kwast Kurt E, Kwon Oh Sung, Laasmaa Martin, Labieniec-Watala Magdalena, Lagarrigue Sylviane, Lai Nicola, Lalic Nebojsa M, Land John M, Lane Nick, Laner Verena, Lanza Ian R, Laouafa Sofien, Laranjinha Joao, Larsen Steen, Larsen Terje S, Lavery Gareth G, Lazou Antigone, Ledo Ana Margarida, Lee Hong Kyu, Leeuwenburgh Christiaan, Lehti Maarit, Lemieux Helene, Lenaz Giorgio, Lerfall Joergen, Li Pingan Andy, Li Puma Lance, Liang Liping, Liepins Edgars, Lin Chien-Te, Liu Jiankang, Lopez Garcia Luis Carlos, Lucchinetti Eliana, Ma Tao, Macedo Maria Paula, Machado Ivo F, Maciej Sarah, MacMillan-Crow Lee Ann, Magalhaes Jose, Magri Andrea, Majtnerova Pavlina, Makarova Elina, Makrecka-Kuka Marina, Malik Afshan N, Marcouiller Francois, Marechal Amandine, Markova Michaela, Markovic Ivanka, Martin Daniel S, Martins Ana Dias, Martins Joao D, Maseko Tumisang Edward, Maull Felicia, Mazat Jean-Pierre, McKenna Helen T, McKenzie Matthew, McMillan Duncan GG, McStay Gavin P, Mendham Amy, Menze Michael A, Mercer John R, Merz Tamara, Messina Angela, Meszaros Andras, Methner Axel, Michalak Slawomir, Mila Guasch Maria, Minuzzi Luciele M, Misirkic Marjanovic Maja, Moellering Douglas R, Moisoi Nicoleta, Molina Anthony JA, Montaigne David, Moore Anthony L, Moore Christy, Moreau Kerrie, Moreira Bruno P, Moreno-Sanchez Rafael, Mracek Tomas, Muccini Anna Maria, Munro Daniel, Muntane Jordi, Muntean Danina M, Murray Andrew James, Musiol Eva, Nabben Miranda, Nair K Sreekumaran, Nehlin Jan O, Nemec Michal, Nesci Salvatore, Neufer P Darrell, Neuzil Jiri, Neviere Remi, Newsom Sean A, Norman Jennifer, Nozickova Katerina, Nunes Sara, Nuoffer Jean-Marc, O'Brien Kristin, O'Brien Katie A, O'Gorman Donal, Olgar Yusuf, Oliveira Ben, Oliveira Jorge, Oliveira Marcus F, Oliveira Marcos Tulio, Oliveira Pedro Fontes, Oliveira Paulo J, Olsen Rolf Erik, Orynbayeva Zulfiya, Osiewacz Heinz D, Paez Hector, Pak Youngmi Kim, Pallotta Maria Luigia, Palmeira Carlos, Parajuli Nirmala, Passos Joao F, Passrugger Manuela, Patel Hemal H, Pavlova Nadia, Pavlovic Kasja, Pecina Petr, Pedersen Tina M, Perales Jose Carles, Pereira da Silva Grilo da Silva Filomena, Pereira Rita, Pereira Susana P, Perez Valencia Juan Alberto, Perks Kara L, Pesta Dominik, Petit Patrice X, Pettersen Nitschke Ina Katrine, Pichaud Nicolas, Pichler Irene, Piel Sarah, Pietka Terri A, Pinho Sonia A, Pino Maria F, Pirkmajer Sergej, Place Nicolas, Plangger Mario, Porter Craig, Porter Richard K, Preguica Ines, Prigione Alessandro, Procaccio Vincent, Prochownik Edward V, Prola Alexandre, Pulinilkunnil Thomas, Puskarich Michael A, Puurand Marju, Radenkovic Filip, Ramzan Rabia, Rattan Suresh IS, Reano Simone, Reboredo-Rodriguez Patricia, Rees Bernard B, Renner-Sattler Kathrin, Rial Eduardo, Robinson Matthew M, Roden Michael, Rodrigues Ana Sofia, Rodriguez Enrique, Rodriguez-Enriquez Sara, Roesland Gro Vatne, Rohlena Jakub, Rolo Anabela Pinto, Ropelle Eduardo R, Roshanravan Baback, Rossignol Rodrigue, Rossiter Harry B, Rousar Tomas, Rubelj Ivica, Rybacka-Mossakowska Joanna, Saada Reisch Ann, Safaei Zahra, Salin Karine, Salvadego Desy, Sandi Carmen, Saner Nicholas, Santos Diana, Sanz Alberto, Sardao Vilma, Sarlak Saharnaz, Sazanov Leonid A, Scaife Paula, Scatena Roberto, Schartner Melanie, Scheibye-Knudsen Morten, Schilling Jan M, Schlattner Uwe, Schmitt Sabine, Schneider Gasser Edith Mariane, Schoenfeld Peter, Schots Pauke C, Schulz Rainer, Schwarzer Christoph, Scott Graham R, Selman 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Tomar Dhanendra, Ton Riccardo, Torp May-Kristin, Torres-Quesada Omar, Towheed Atif, Treberg Jason R, Tretter Laszlo, Trewin Adam J, Trifunovic Aleksandra, Trivigno Catherine, Tronstad Karl Johan, Trougakos Ioannis P, Truu Laura, Tuncay Erkan, Turan Belma, Tyrrell Daniel J, Urban Tomas, Urner Sofia, Valentine Joseph Marco, Van Bergen Nicole J, Van der Ende Miranda, Varricchio Frederick, Vaupel Peter, Vella Joanna, Vendelin Marko, Vercesi Anibal E, Verdaguer Ignasi Bofill, Vernerova Andrea, Victor Victor Manuel, Vieira Ligo Teixeira Camila, Vidimce Josif, Viel Christian, Vieyra Adalberto, Vilks Karlis, Villena Josep A, Vincent Vinnyfred, Vinogradov Andrey D, Viscomi Carlo, Vitorino Rui Miguel Pinheiro, Vlachaki Walker Julia, Vogt Sebastian, Volani Chiara, Volska Kristine, Votion Dominique-Marie, Vujacic-Mirski Ksenija, Wagner Brett A, Ward Marie Louise, Warnsmann Verena, Wasserman David H, Watala Cezary, Wei Yau-Huei, Weinberger Klaus M, Weissig Volkmar, White Sarah Haverty, Whitfield Jamie, Wickert Anika, Wieckowski Mariusz R, Wiesner Rudolf J, Williams Caroline M, Winwood-Smith Hugh, Wohlgemuth Stephanie E, Wohlwend Martin, Wolff Jonci Nikolai, Wrutniak-Cabello Chantal, Wuest Rob CI, Yokota Takashi, Zablocki Krzysztof, Zanon Alessandra, Zanou Nadege, Zaugg Kathrin, Zaugg Michael, Zdrazilova Lucie, Zhang Yong, Zhang Yizhu, Zikova Alena, Zischka Hans, Zorzano Antonio, Zujovic Tijana, Zurmanova Jitka, Zvejniece Liga
- Subjects
uncoupling ,MitoPedia: Respiratory states, SI - The International System of Units, IUPAC, Coupling control, Mitochondrial preparations, Protonmotive force, Uncoupling, Oxidative phosphorylation, Phosphorylation efficiency, Electron transfer-pathway, LEAK-respiration, Residual oxygen consumption, Normalization of rate, Flow, Flux, Flux control ratio, Mitochondrial marker, Cell count, Oxygen ,[SDV]Life Sciences [q-bio] ,coupling control ,protonmotive force ,oxidative phosphorylation ,mitochondrial respiratory control ,State 4 ,electron transfer ,State 2 ,State 3 ,Mitochondrial physiology ,residual oxygen consumption ,flux ,normalization ,ion leak and slip compensatory state ,efficiency ,electron transfer system ,flow ,mitochondrial physiology ,oxygen ,mitochondrial preparations ,proton leak - Abstract
As the knowledge base and importance of mitochondrial physiology to evolution, health and diseaseexpands, the necessity for harmonizing the terminologyconcerning mitochondrial respiratory states and rates has become increasingly apparent. Thechemiosmotic theoryestablishes the mechanism of energy transformationandcoupling in oxidative phosphorylation. Theunifying concept of the protonmotive force providestheframeworkfordeveloping a consistent theoretical foundation ofmitochondrial physiology and bioenergetics.We followthe latest SI guidelines and those of the International Union of Pure and Applied Chemistry(IUPAC)onterminology inphysical chemistry, extended by considerationsofopen systems and thermodynamicsof irreversible processes.Theconcept-driven constructive terminology incorporates the meaning of each quantity and alignsconcepts and symbols withthe nomenclature of classicalbioenergetics. We endeavour to provide a balanced view ofmitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes.Uniform standards for evaluation of respiratory states and rates will ultimatelycontribute BEC 2020.1 doi:10.26124/bec:2020-0001.v1www.bioenergetics-communications.org3of 44to reproducibility between laboratories and thussupport the development of datarepositoriesof mitochondrial respiratory function in species, tissues, and cells.Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery.
- Published
- 2020
37. Metabolic Memory in Diabetes – Mechanistic Insights and the Impact of Cardiovascular Medication
- Author
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Sosdean, Raluca, primary, Ionica, Loredana N., additional, Merce, Adrian P., additional, Muntean, Danina M., additional, and Sturza, Adrian, additional
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- 2021
- Full Text
- View/download PDF
38. Thrombospondin-1 Serum Levels In Hypertensive Patients With Endothelial Dysfunction After One Year Of Treatment With Perindopril
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Buda, Valentina, Andor, Minodora, Cristescu, Carmen, Tomescu, Mirela Cleopatra, Muntean, Danina M, Bâibâță, Dana Emilia, Bordejevic, Diana Aurora, Danciu, Corina, Dalleur, Olivia, Coricovac, Dorina, Crainiceanu, Zorin, Tudor, Anca, Ledeti, Ionut, Petrescu, Lucian, UCL - SSS/LDRI - Louvain Drug Research Institute, and UCL - (SLuc) Département de pharmacie
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Pharmacology ,Male ,Drug Design, Development and Therapy ,ACE inhibitors ,essential arterial hypertension ,Pharmaceutical Science ,Blood Pressure ,Middle Aged ,Thrombospondin 1 ,endothelial function ,Echocardiography ,Drug Discovery ,Hypertension ,Perindopril ,TSP-1 ,Humans ,Female ,Endothelium, Vascular ,Antihypertensive Agents ,Original Research - Abstract
Valentina Buda,1,* Minodora Andor,2,* Carmen Cristescu,1,* Mirela Cleopatra Tomescu,2 Danina M Muntean,3 Dana Emilia BâibâÈÄ,4,5 Diana Aurora Bordejevic,4,5 Corina Danciu,6 Olivia Dalleur,7 Dorina Coricovac,8 Zorin Crainiceanu,9 Anca Tudor,10 Ionut Ledeti,11 Lucian Petrescu4,5 1Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 2Department of Medical Semiotics, Faculty of Medicine, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 3Department of Pathophysiology, Faculty of Medicine, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 4Department of Cardiology VI, Faculty of Medicine, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 5Cardiovascular Diseases Institute, Timisoara 300310, Romania; 6Department of Pharmacognosy, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 7Clinical Pharmacy Research Group, Louvain Drug Research Institute, Université Catholique De Louvain, Woluwe-Saint-Lambert 1200, Bruxelles, Belgium; 8Department of Toxicology, Faculty of Pharmacy, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 9Department of Plastic and Reconstructive Surgery, Faculty of Medicine, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 10Department of Statistics and Biomedical Informatics, Faculty of Medicine, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania; 11Department of Physical Chemistry, Faculty of Pharmacy, “Victor BabeÅ” University of Medicine and Pharmacy, Timisoara 300041, Romania*These authors contributed equally to this workCorrespondence: Valentina BudaCorina Danciu Faculty of Pharmacy, “Victor BabeÅ” University of Medicine and Pharmacy, 2 Eftimie Murgu Street, Timisoara 300041, RomaniaTel +40-256-494-604Fax +40-256-494-604Email buda.valentina.oana@gmail.comBackground: Thrombospondin-1 (TSP-1) is a matricellular functional protein of the extracellular matrix. As it is not constitutively present extracellularly, its secretion is enhanced in several situations, namely injury, chronic pathology, tissue remodeling, angiogenesis, and aging. Over the last decade, TSP-1 has been reported to be involved in complex and opposing biological effects on vasculature in the context of NO signaling. Several studies have reported high patient TSP-1 plasma levels, indicating that the protein can potentially serve as a prognostic marker for pulmonary arterial hypertension.Materials and methods: Here, we aimed to quantify TSP-1 serum levels in hypertensive patients with endothelial dysfunction before and after one year of treatment with Perindopril (an antihypertensive drug with vasoprotective properties).Results: After one year of treatment, TSP-1 levels increased in hypertensive patients compared to baseline (T0: 8061.9 ± 3684.80 vs T1: 15380±5887 ng/mL, p
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- 2019
39. Cardioprotection against myocardial reperfusion injury: successes, failures, and perspectives
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Duicu, Oana M., Angoulvant, Denis, and Muntean, Danina M.
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Genetic translation -- Research ,Reperfusion injury -- Physiological aspects -- Genetic aspects ,Myocardial ischemia -- Physiological aspects -- Genetic aspects ,Biological sciences - Abstract
The past few decades have witnessed an enormous number of research strategies aimed at protecting the heart against myocardial ischemia-reperfusion injury. Several randomized clinical trials are nowadays in progress testing whether promising therapeutic strategies aimed at preventing lethal reperfusion injury can be translated from bench to bedside. Many of these interventions, either pharmacological or mechanical, are targeting mitochondria as the final effectors of cardioprotection. Despite encouraging pre-clinical studies and small proof of concept clinical trials, there are still several limitations that may jeopardize the efficacy of cardioprotective strategies. These limitations include clinical setting, patient profile, drug administration, and methods for evaluating treatment efficacy. Identifying potential mechanistic and methodological pitfalls in the field may improve future translational research. Key words: ischemia-reperfusion injury, cardioprotection, conditioning, translation, mitochondria. La derniere decennie a ete temoin du developpement d'un grand nombre de strategies de recherche visant a proteger le coeur du dommage d'ischemie-reperfusion myocardique. Plusieurs essais cliniques aleatoires sont actuellement en cours, afin de determiner si des strategies therapeutiques prometteuses visant a prevenir un dommage de reperfusion letal peuvent etre transferees de la paillasse au patient. Plusieurs de ces interventions, qu'elles soient pharmacologiques ou mecaniques, ciblent les mitochondries comme effecteurs finaux de la cardioprotection. Malgre les etudes precliniques et les petits essais cliniques de demonstration de faisabilite encourageants, il existe encore plusieurs limitations qui peuvent mettre en peril l'efficacite des strategies de cardioprotection. Ces limitations incluent le contexte clinique, le profil du patient, l'administration de medicaments et les methodes d'evaluation d'efficacite du traitement. L'identification des ecueils mecaniques et methodologiques potentiels dans ce domaine peut ameliorer la recherche translationnelle future. [Traduit par la Redaction] Mots-cles : dommage d'ischemie-reperfusion, cardioprotection, conditionnement, transfert, mitochondrie., Introduction Cardiovascular diseases, and in particular, coronary heart disease, remain the number one cause of death worldwide and have rapidly risen in prevalence in the past few years in the [...]
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- 2013
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40. Ageing-induced decrease in cardiac mitochondrial function in healthy rats
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Duicu, Oana M., Mirica, Silvia N., Gheorgheosu, Dorina E., Privistirescu, Andreea I., Fira-Mladinescu, Ovidiu, and Muntean, Danina M.
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Aging -- Health aspects ,Membrane proteins -- Physiological aspects -- Health aspects ,Reactive oxygen species -- Physiological aspects -- Health aspects ,Biological sciences - Abstract
It is widely recognized that mitochondrial dysfunction is a key component of the multifactorial process of ageing. The effects of age on individual components of mitochondrial function vary across species and strains. In this study we investigated the oxygen consumption, the mitochondrial membrane potential (Δψ), the sensitivity of mitochondrial permeability transition pore (mPTP) to calcium overload, and the production of reactive oxygen species (ROS) in heart mitochondria isolated from old compared with adult healthy Sprague-Dawley rats. Respirometry studies and Δψ measurements were performed with an Oxygraph-2k equipped with a tetraphenylphosphonium electrode. ROS production and calcium retention capacity were measured spectrofluorimetrically. Our results show an important decline for all bioenergetic parameters for both complex I and complex II supported-respiration, a decreased Δψ in mitochondria energized with complex I substrates, and an increased mitochondrial ROS production in the old compared with the adult group. Mitochondrial sensitivity to [Ca.sup.2+]-induced mPTP opening was also increased in the old compared with the adult animals. Moreover, the protective effect of cyclosporine A on mPTP opening was significantly reduced in the old group. We conclude that healthy ageing is associated with a decrease in heart mitochondria function in Sprague-Dawley rats. Key words: ageing, oxidative phosphorylation, reactive oxygen species, calcium retention capacity. Il est generalement reconnu que la dysfonction mitochondriale est une composante cle du processus multifactoriel qu'est le vieillissement. Les effets de l'age sur les composantes individuelles de la fonction mitochondriale varient en fonction des especes et des souches. Dans cette etude, nous avons examine et compare la consommation d'oxygene, le potentiel membranaire (Δψ), la sensibilite du pore de transition de permeabilite mitochondriale (PTPM) a une surcharge en calcium et la production d'especes reactives d'oxygene (ERO) des mitochondries du coeur isolees de rats en sante Sprague-Dawley (SD) adultes vs ages. Les etudes en respirometrie et les mesures du Δψ ont ete realisees avec un Oxygraph-2k equipe d'une electrode au tetraphenylphosphonium. La production d'ERO et la capacite de retention du calcium (CRC) ont ete mesurees par spectrofluorometrie. Nos resultats ont montre un declin important de tous les parametres bioenergetiques de la respiration au niveau des complexes I et II, une diminution du Δψ dans les mitochondries tirant leur energie des substrats du complexe I et un accroissement de la production d'ERO mitochondriales chez le groupe age comparativement au groupe adulte. La sensibilite du PTPM a l'ouverture induite par le calcium etait aussi accrue chez les animaux ages comparativement aux adultes. De plus, l'effet protecteur de la cyclosporine A sur l'ouverture du PTPM etait significativement reduite chez le groupe age. En conclusion, le vieillissement normal est associe a la reduction de la fonction des mitochondries du coeur chez les rats Sprague-Dawley. [Traduit par la Redaction] Mots-cles: vieillissement, phosphorylation oxydative, especes reactives d'oxygene, capacite de retention du calcium., Introduction Ageing is the inexorable process of gradual decrease in body functional capacity, for which the underlying molecular basis remains largely elusive. It has been widely accepted that the functional [...]
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- 2013
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41. L-364,373 (R-L3) enantiomers have opposite modulating effects on [I.sub.Ks] in mammalian ventricular myocytes
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Corici, Claudia, Kohajda, Zsofia, Kristof, Attila, Horvath, Andras, Virag, Laszlo, Szel, Tamas, Nagy, Norbert, Szakonyi, Zsolt, Fulop, Ferenc, Muntean, Danina M., Varro, Andras, and Jost, Norbert
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Heart cells -- Physiological aspects -- Health aspects ,Arrhythmia -- Physiological aspects ,Heart ventricle, Left -- Physiological aspects -- Health aspects ,Biological sciences - Abstract
Activators of the slow delayed rectifier [K.sup.+] current ([I.sub.Ks]) have been suggested as promising tools for suppressing ventricular arrhythmias due to prolongation of repolarization. Recently, L-364,373 (R-L3) was nominated to activate [I.sub.Ks] in myocytes from several species; however, in some studies, it failed to activate [I.sub.Ks]. One later study suggested opposite modulating effects from the R-L3 enantiomers as a possible explanation for this discrepancy. Therefore, we analyzed the effect of the RL-3 enantiomers on [I.sub.Ks] in ventricular mammalian myocytes, by applying standard microelectrode and whole-cell patch- clamp techniques at 37°C. We synthesized 2 substances, ZS_1270B (right) and ZS_1271B (left), the 2 enantiomers of R- L3. In rabbit myocytes, ZS_1270B enhanced the [I.sub.Ks] tail current by approximately 30%, whereas ZS_1271B reduced [I.sub.Ks] tails by 45%. In guinea pig right ventricular preparations, ZS_1270B shortened [APD.sub.90] (action potential duration measured at 90% repolarization) by 12%, whereas ZS_1271B lengthened it by approximately 15%. We concluded that R-L3 enantiomers in the same concentration range indeed have opposite modulating effects on [I.sub.Ks], which may explain why the racemic drug R-L3 previously failed to activate [I.sub.Ks]. ZS_1270B is a potent [I.sub.Ks] activator, therefore, this substance is appropriate to test whether [I.sub.Ks] activators are ideal tools to suppress ventricular arrhythmias originating from prolongation of action potentials. Key words: L-364,373, slow delayed rectifier potassium current, [I.sub.Ks] activator, [I.sub.Ks] blocker, enantiomers, antiarrhythmic drugs. On a suggere que les activateurs du courant potassique rectifiant retarde lent ([I.sub.Ks]) soient des outils prometteurs pour supprimer les arythmies ventriculaires causees par la prolongation de la repolarisation. Recemment, le L-364,373 (R-L3) a ete identifie comme activateur du [I.sub.Ks] dans les myocytes de plusieurs especes ; toutefois, dans certaines etudes, il ne parvenait pas a activer le [I.sub.Ks]. Une etude ulterieure a suggere que les effets modulateurs opposes d'enantiomeres du R-L3 pourraient peut-etre expliquer cette divergence. Nous avons ainsi analyse l'effet d'enantiomeres de R-L3 sur le [I.sub.Ks] dans des myocytes ventriculaires de mammifere, en utilisant la technique standard de microelectrode et de patch clamp sur cellule entiere a 37°C. Nous avons synthetise deux substances, le ZS_1270B (droit) et le ZS_1271B (gauche), les deux enantiomeres du R-L3. Le ZS_1270B accroissait le courant [I.sub.Ks] de queue d'environ 30 % alors que le ZS_1271B reduisait les queues du [I.sub.Ks] de 45 %. Dans les preparations ventriculaires droites du cobaye, le ZS_1270B raccourcissait [l'APD.sub.90] de 12 % alors que le ZS_1271B l'allongeait inversement de 15 %. Nous avons conclu que les enantiomeres du R-L3 possedent effectivement des effets modulateurs opposes, ce qui peut expliquer pourquoi le melange racemique du medicament RL-3 ne parvenait pas a activer le [I.sub.Ks]. Le ZS_1270B est un puissant activateur du [I.sub.Ks] : consequemment, cette substance convient pour tester si les activateurs de [I.sub.Ks] sont effectivement des outils ideaux pour supprimer les arythmies ventriculaires emanant de la prolongations des potentiels d'action. [Traduit par la Redaction] Mots-cles: L-364,373, courant potassique rectifiant retarde lent, activateur du [I.sub.Ks], bloqueur du [I.sub.Ks], enantiomeres, medicaments anti-arythmiques., Introduction Action potential repolarization is an important phenomenon in the heart, where it controls action potential duration (APD) and thus affects refractoriness and conduction of electrical impulses throughout the heart. [...]
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- 2013
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42. Magnesium orotate elicits acute cardioprotection at reperfusion in isolated and in vivo rat hearts
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Mirica, Silvia N., Duicu, Oana M., Trancota, Simona L., Fira-Mladinescu, Ovidiu, Angoulvant, Denis, and Muntean, Danina M.
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Heart attack -- Risk factors -- Diagnosis -- Care and treatment -- Research ,Magnesium compounds -- Health aspects -- Research ,Reperfusion (Physiology) -- Research ,Biological sciences - Abstract
Orotic acid and its salts chronically administered have been shown to significantly improve cardiac function in pathological settings associated with ischemia-reperfusion (I/R) injury. The aim of our study was to investigate the effect of magnesium orotate (Mg-Or) administration at the onset of post-ischemic reperfusion on myocardial function and infarct size (IS). Ex-vivo experiments performed on isolated perfused rat hearts were used to compare Mg-Or administration with a control group (buffer treated), ischemic post-conditioning, orotic acid treatment, and Mg[Cl.sub.2] treatment. Mg-Or administration was also investigated in an in-vivo model of regional I/R performed in rats undergoing reversible coronary ligation. The effect of Mg-Or on mitochondrial permeability transition pore (mPTP) opening after I/R was investigated in vitro to gain mechanistic insights. Both ex-vivo and in-vivo experiments showed a beneficial effect from Mg-Or administration at the onset of reperfusion on myocardial function and IS. In-vitro assays showed that Mg-Or significantly delayed mPTP opening after I/R. Our data suggest that Mg-Or administered at the very onset of reperfusion may preserve myocardial function and reduce IS. This beneficial effect may be related to a significant reduction of mPTP opening, a usual trigger of cardiac cell death following I/R. Key words: magnesium orotate, cardioprotection, ischemia-reperfusion, ischemic post-conditioning, in vivo. L'administration au long cours d'acide orotique ou de ses sels a montre un effet benefique sur la fonction cardiaque dans plusieurs situations pathologiques associees aux lesions d'ischemie-reperfusion (I/R). L'objectif de notre etude etait d'evaluer l'effet de l'orotate de magnesium (Mg-Or) administre en tout debut de reperfusion myocardique post ischemique sur la taille d'infarctus (TI) et la fonction cardiaque. Un modele ex vivo d'I/R sur cceur isole perfuse de rats a compare l'administration de Mg-Or avec les groupes experimentaux control (tampon), post conditionnement ischemique, acide orotique, et Mg[Cl.sub.2]. L'effet de Mg-Or a egalement ete evalue sur un modele in vivo d'I/R myocardique regional par ligature coronaire chez le rat. Une etude mecanistique a evalue l'effet de Mg-Or sur l'ouverture du port de permeabilite de transition mitochondriale (mPTP). L'administration de Mg-Or en debut de reperfusion sur les modeles ex vivo et in vivo entrame une diminution de la TI et une preservation de la fonction cardiaque. L'etude mecanistique montre que Mg-Or retarde l'ouverture du mPTP apres I/R myocardique. Nos resultats suggerent que Mg-Or administre en debut de reperfusion est susceptible de diminuer la TI et de preserver la fonction cardiaque. Cet effet est vraisemblablement lie a son action inhibitrice sur l'ouverture du mPTP, phenomene implique dans les processus de mort cellulaire post I/R myocardique. Mots-cles: orotate de magnesium, cardioprotection, ischemie-reperfusion, post conditionnement ischemique, in vivo., Introduction Myocardial infarction represents a major cause of morbidity and mortality worldwide. The cornerstone of treatment is represented by timely restoration of coronary reperfusion achieved either pharmacologically by thrombolysis and [...]
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- 2013
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43. Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Statin Toxicity
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Avram, Vlad F., Chamkha, Imen, Åsander-Frostner, Eleonor, Ehinger, Johannes K., Timar, Romulus Z., Hansson, Magnus J., Muntean, Danina M., and Elmér, Eskil
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Adult ,Blood Platelets ,Male ,Cell Respiration ,NV118 ,Succinic Acid ,nutritional and metabolic diseases ,Article ,statins ,mitochondria ,lcsh:Chemistry ,Oxygen Consumption ,lcsh:Biology (General) ,lcsh:QD1-999 ,platelets ,Humans ,Female ,lipids (amino acids, peptides, and proteins) ,cardiovascular diseases ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,HepG2 cells ,lcsh:QH301-705.5 ,cell-permeable succinate ,Aged - Abstract
Statins are the cornerstone of lipid-lowering therapy. Although generally well tolerated, statin-associated muscle symptoms (SAMS) represent the main reason for treatment discontinuation. Mitochondrial dysfunction of complex I has been implicated in the pathophysiology of SAMS. The present study proposed to assess the concentration-dependent ex vivo effects of three statins on mitochondrial respiration in viable human platelets and to investigate whether a cell-permeable prodrug of succinate (complex II substrate) can compensate for statin-induced mitochondrial dysfunction. Mitochondrial respiration was assessed by high-resolution respirometry in human platelets, acutely exposed to statins in the presence/absence of the prodrug NV118. Statins concentration-dependently inhibited mitochondrial respiration in both intact and permeabilized cells. Further, statins caused an increase in non-ATP generating oxygen consumption (uncoupling), severely limiting the OXPHOS coupling efficiency, a measure of the ATP generating capacity. Cerivastatin (commercially withdrawn due to muscle toxicity) displayed a similar inhibitory capacity compared with the widely prescribed and tolerable atorvastatin, but did not elicit direct complex I inhibition. NV118 increased succinate-supported mitochondrial oxygen consumption in atorvastatin/cerivastatin-exposed platelets leading to normalization of coupled (ATP generating) respiration. The results acquired in isolated human platelets were validated in a limited set of experiments using atorvastatin in HepG2 cells, reinforcing the generalizability of the findings.
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- 2021
44. Pleiotropic Effects of Eugenol: The Good, the Bad, and the Unknown
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Aburel, Oana M., Pavel, Ioana Z., Dănilă, Maria D., Lelcu, Theia, Roi, Alexandra, Lighezan, Rodica, Muntean, Danina M., and Rusu, Laura C.
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Article Subject - Abstract
Phytocompounds and medicinal herbs were used in traditional ancient medicine and are nowadays increasingly screened in both experimental and clinical settings due to their beneficial effects in several major pathologies. Similar to the drug industry, phytotherapy is interested in using nanobased delivery systems to view the identification and characterization of the cellular and molecular therapeutic targets of plant components. Eugenol, the major phenolic constituent of clove essential oil, is a particularly versatile phytochemical with a vast range of therapeutic properties, among which the anti-inflammatory, antioxidant, and anticarcinogenic effects have been systematically addressed. In the past decade, with the emerging understanding of the role of mitochondria as critical organelles in the pathophysiology of noncommunicable diseases, research regarding the role of phytochemicals as modulators of bioenergetics and metabolism is on a rise. Here, we present a brief overview of the major pharmacological properties of eugenol, with special emphasis on its applications in dental medicine, and provide preliminary data regarding its effects, alone, and included in polyurethane nanostructures, on mitochondrial bioenergetics, and glycolysis in human HaCaT keratinocytes.
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- 2021
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45. Metabolomics in Chronic Kidney Diseases: Here to Stay
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Pătruică, Mihaela-Roxana, primary, Gădălean, Florica, additional, Vlad, Adrian, additional, Sturza, Adrian, additional, Jianu, Dragos Cătălin, additional, Balint, Lavinia, additional, Ienciu, Silvia, additional, Petrica, Ligia, additional, Muntean, Danina M., additional, and Socaciu, Carmen, additional
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- 2021
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46. Volatile anaesthetics and cardioprotection – lessons from animal studies
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Muntean, Danina M., Ordodi, Valentin, Ferrera, René, and Angoulvant, Denis
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- 2013
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47. Angiotensin-Converting-Enzyme 2 and SARS-CoV2: A Dangerous Liaison
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Sturza, Adrian, primary, Marian, Cătălin V., additional, Muntean, Danina M., additional, and Crețu, Octavian M., additional
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- 2020
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48. Monoamine Oxidase-Related Vascular Oxidative Stress in Diseases Associated with Inflammatory Burden
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Sturza, Adrian, Popoiu, Călin M., Ionică, Mihaela, Duicu, Oana M., Olariu, Sorin, Muntean, Danina M., and Boia, Eugen S.
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Article Subject - Abstract
Monoamine oxidases (MAO) with 2 isoforms, A and B, located at the outer mitochondrial membrane are flavoenzyme membranes with a major role in the metabolism of monoaminergic neurotransmitters and biogenic amines in the central nervous system and peripheral tissues, respectively. In the process of oxidative deamination, aldehydes, hydrogen peroxide, and ammonia are constantly generated as potential deleterious by-products. While being systematically studied for decades as sources of reactive oxygen species in brain diseases, compelling evidence nowadays supports the role of MAO-related oxidative stress in cardiovascular and metabolic pathologies. Indeed, oxidative stress and chronic inflammation are the most common pathomechanisms of the main noncommunicable diseases of our century. MAO inhibition with the new generation of reversible and selective drugs has recently emerged as a pharmacological strategy aimed at mitigating both processes. The aim of this minireview is to summarize available information regarding the contribution of MAO to the vascular oxidative stress and endothelial dysfunction in hypertension, metabolic disorders, and chronic kidney disease, all conditions associated with increased inflammatory burden.
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- 2019
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49. Mitochondrial respiratory states and rates
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Gnaiger, Erich, Aasander Frostner, Eleonor, Abdul Karim, Norwahidah, Abumrad, Nada A, Acuna-Castroviejo, Dario, Adiele, Reginald C, Ahn, Bumsoo, Ali, Sameh S, Alton, Lesley, Alves, Marco G, Amati, Francesca, Amoedo, Nivea Dias, Andreadou, Ioanna, Arago, Marc, Aral, Cenk, Arandarcikaite, Odeta, Armand, Anne-Sophie, Arnould, Thierry, Avram, Vlad Florian, Bailey, Damian M, Bajpeyi, Sudip, Bajzikova, Martina, Bakker, Barbara M, Barlow, Jonathan, Bastos Sant'Anna Silva, Ana Carolina, Batterson, Philip, Battino, Maurizio, Bazil, Jason, Beard, Daniel A, Bednarczyk, Piotr, Bello, Fiona, Ben-Shachar, Dorit, Bergdahl, Andreas, Berge, Rolf K, Bergmeister, Lisa, Bernardi, Paolo, Berridge, Michael V, Bettinazzi, Stefano, Bishop, David, Blier, Pierre U, Blindheim, Dan Filip, Boardman, Neoma T, Boetker, Hans Erik, Borchard, Sabine, Boros, Mihaly, Borsheim, Elisabet, Borutaite, Vilma, Botella, Javier, Bouillaud, Frederic, Bouitbir, Jamal, Boushel, Robert C, Bovard, Josh, Breton, Sophie, Brown, David A, Brown, Guy C, Brown, Robert A, Brozinick, Joseph T, Buettner, Garry R, Burtscher, Johannes, Calabria, Elisa, Calbet, Jose A, Calzia, Enrico, Cannon, Daniel T, Cano Sanchez, Maria, Canto Alvarez, Carlos, Cardoso, Luiza Helena Daltro, Carvalho, Eugenia, Casado Pinna, Marta, Cassar, Samantha, Cassina, Adriana M, Castelo, Maria P, Gonzalez-Franquesa, A, Cavalcanti-de-Albuquerque, Joao Paulo, Cervinkova, Zuzana, Chabi, Beatrice, Chakrabarti, Lisa, Chakrabarti, Sasanka, Chaurasia, Bhagirath, Chen, Qi, Chicco, Adam J, Chinopoulos, Christos, Chowdhury, Subir K, Cizmarova, Beata, Clementi, Emilio, Coen, Paul M, Cohen, Bruce H, Coker, Robert H, Collin, Anne, Crisostomo, Luis, Dahdah, Norma, Dalgaard, Louise T, Dambrova, Maija, Danhelovska, Tereza, Darveau, Charles A, Das, Anibh M, Dash, Ranjan K, Davidova, Eliska, Davis, Michael S, De Goede, Paul, De Palma, Clara, Dembinska-Kiec, Aldona, Detraux, Damien, Devaux, Yvan, Di Marcello, Marco, Dias, Tania R, Distefano, Giovanna, Doermann, Niklas, Doerrier, Carolina, Dong, Lan-Feng, Donnelly, Chris, Drahota, Zdenek, Duarte, Filipe Valente, Dubouchaud, Herve, Duchen, Michael R, Dumas, Jean-Francois, Durham, William J, Dymkowska, Dorota, Dyrstad, Sissel E, Dyson, Alex, Dzialowski, Edward M, Eaton, Simon, Ehinger, Johannes, Elmer, Eskil, Endlicher, Rene, Engin, Ayse B, Escames, Germaine, Ezrova, Zuzana, Falk, Marni Joy, Fell, David A, Ferdinandy, Peter, Ferko, Miroslav, Ferreira, Julio Cesar Batista, Ferreira, Rita, Ferri, Alessandra, Fessel, Joshua P, Filipovska, Aleksandra, Fisar, Zdenek, Fischer, Christine, Fischer, Michael, Fisher, Gordon, Fisher, Joshua J, Ford, Ellen, Fornaro, Mara, Galina, Antonio, Galkin, Alexander, Gallee, Leon, Galli, Gina L, Gama Perez, Pau, Gan, Zhenji, Ganetzky, Rebecca, Garcia-Rivas, Gerardo, Garcia-Roves, Pablo Miguel, Garcia-Souza, Luiz Felipe, Garipi, Enis, Garlid, Keith D, Garrabou, Gloria, Garten, Antje, Gastaldelli, Amalia, Gayen, Jiaur, Genders, Amanda J, Genova, Maria Luisa, Giovarelli, Matteo, Goncalo Teixeira da Silva, Rui, Goncalves, Debora Farina, Gonzalez-Armenta, Jenny L, Gonzalez-Freire, Marta, Gonzalo, Hugo, Goodpaster, Bret H, Gorr, Thomas A, Gourlay, Campbell W, Granata, Cesare, Grefte, Sander, Guarch, Meritxell Espino, Gueguen, Naig, Gumeni, Sentiljana, Haas, Clarissa B, Haavik, Jan, Haendeler, Judith, Haider, Markus, Hamann, Andrea, Han, Jin, Han, Woo Hyun, Hancock, Chad R, Hand, Steven C, Handl, Jiri, Hargreaves, Ian P, Harper, Mary Ellen, Harrison, David K, Hassan, Hazirah, Hausenloy, Derek J, Heales, Simon JR, Heiestad, Christina, Hellgren, Kim T, Hepple, Russell T, Hernansanz-Agustin, Pablo, Hewakapuge, Sudinna, Hickey, Anthony J, Ho, Dieu Hien, Hoehn, Kyle L, Hoel, Frederik, Holland, Olivia J, Holloway, Graham P, Hoppel, Charles L, Hoppel, Florian, Houstek, Josef, Huete-Ortega, Maria, Hyrossova, Petra, Iglesias-Gonzalez, Javier, Irving, Brian A, Isola, Raffaella, Iyer, Shilpa, Jackson, Christophe B, Jadiya, Pooja, Jana, Prado Fabian, Jang, David H, 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- Subjects
uncoupling ,Mitochondrial respiratory control ,coupling control ,protonmotive force ,oxidative phosphorylation ,mitochondrial respiratory control ,NARILIS ,ET [electron transfer] ,electron transfer ,residual oxygen consumption ,flux ,normalization ,efficiency ,flow ,oxygen ,mitochondrial preparations ,proton leak - Abstract
As the knowledge base and importance of mitochondrial physiology to human health expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow guidelines of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of databases of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery.
- Published
- 2019
- Full Text
- View/download PDF
50. Formulation and Characterization of Polyurethane Microstructures with Propolis Extract
- Author
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Duca, Alexandra, primary, Borcan, Florin, additional, Muntean, Danina M., additional, Alexa, Ersilia C., additional, and Soica, Codruta M., additional
- Published
- 2019
- Full Text
- View/download PDF
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