5 results on '"Danila, Maria D."'
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2. 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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3. 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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4. 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.
- Subjects
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 [...]
- Published
- 2015
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5. 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 [...]
- Published
- 2015
- Full Text
- View/download PDF
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