Rozprawy doktorskie na temat „Nicotinamide adenine dinucleotide”
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Moideen, Abdul Nazeer. "Nicotinamide adenine dinucleotide biosynthesis enzymes in rheumatoid arthritis". Thesis, Cardiff University, 2016. http://orca.cf.ac.uk/97161/.
Pełny tekst źródłaStevenson, Eileen C. "The utilisation of fibre-entrapped cells within a novel bioreactor for the production of NADH". Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334643.
Pełny tekst źródłaTrammell, Samuel A. J. "Novel NAD+ metabolomic technologies and their applications to Nicotinamide Riboside interventions". Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3203.
Pełny tekst źródłaAl, Ghouleh Imad 1977. "The role of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase in endothelial activation in sepsis /". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115854.
Pełny tekst źródłaExpression of a gene can be increased by a rise in transcription as well as post-transcriptional changes, such as mRNA stability modifications. We assessed the role of NADPH oxidase in this process and found a complex interaction. Although LPS increases IL-8 transcription, it also destabilizes IL-8 mRNA in a p38 and extracellular signal-regulated kinase (ERK) MAPK dependent manner, which was only evident after blocking NADPH oxidase. This regulation involved the mRNA de-stabilizing factor tristetraprolin (TTP). In contrast, TNF-alpha enhanced the stability of IL-8, IL-6 and ICAM-1 mRNA in a p38 MAPK dependent, but NADPH oxidase independent manner. Furthermore, LPS did not have an effect on mRNA stability of IL-6 or ICAM-1 in our system. Thus, we conclude from our studies that the NAPDH oxidase is important for the induction of inflammatory molecules in LPS and TNF-alpha treated EC and is also involved in mRNA stability regulation of these molecules in a signal and gene specific fashion.
Pergolizzi, Giulia. "Novel derivatives of nicotinamide adenine dinucleotide (NAD) and their biological evaluation against NAD-consuming enzymes". Thesis, University of East Anglia, 2012. https://ueaeprints.uea.ac.uk/42447/.
Pełny tekst źródłaBalico, Laís de Lourdes de Lima. "Caracterização molecular e bioquímica de um transportador mitocondrial de nicotinamida adenina dinucleotídeo de Aspergillus fumigatus". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-17042015-135749/.
Pełny tekst źródłaThe A. fumigatus is a saprophytic fungus and is a major opportunistic pathogen in immunosuppressed patients. Previous studies in our lab has showed that mitochondrias of the P. brasiliensis and A. fumigatus, NAD+ is able to induce the formation of mitochondrial membrane potential, which could be dissipated by FCCP, suggesting the presence of a NAD+/NADH carrier as described in S. cerevisiae. Using bioinformatics tools, it was identified in Aspergillus Gene database a sequence containing 32% of identity with the gene ndt1p of S. cerevisiae. A fragment of cDNA was obtained from the ndt1p mRNA sequence, containing 1194 bp by using PCR-overlaping and cloned in pGEM®-T Easy vector. Then, the sequence was subcloned in pET28-a(+) vector and expressed in E. coli BL21 (DE3). The recombinant protein was purified from inclusion bodies and the identity confirmed by mass spectrometry and by Western Blotting using anti-His-tag antibody. The recombinant protein was used to produce polyclonal antibody anti-Ndt1 in rabbit. For expression in yeast, the ndt1 cDNA of A. fumigatus was subcloned into pYES2 vector and the yeast S. cerevisiae ?ndt1?ndt2 were transformed. Growth curve and induction of the recombinant protein expression Ndt1 was performed and the protein was detected using a polyclonal anti-Ndt1 antibody after 16 hours of expression. During this period it was found that the yeast were in exponential growth phase. The double mutant strain shows a slower growth rate compared to the strain expressing the recombinant protein growth rate when grown in fermentable medium. The isolated mitochondria from both strains were subjected to measurement of the membrane potential which showed coupling between substrate oxidation and oxidative phosphorylation. Furthermore, these measurements evidenced that the strain expressing the recombinant protein NAD+ induced the formation of a membrane potential larger than the control strain. The transport NAD+ was evaluated and showed that the strain expressing the protein Ndt1 has an increase in NADH fluorescence, indicating that NAD+ was able to enter into the mitochondrial matrix and then reduced to NADH by enzymes from the matrix. The determination of the production of reactive oxygen species was performed using the fluorescent probe CM-H2DCFDA and MitoSox Red in spheroplasts of the yeast S. cerevisiae. Both experiments showed no significant difference between the strain expressing Ndt1 protein and strain control. The carbonylated proteins levels were checked using anti-DNP, after the reaction with dinitrophenylhydrazone and there is no significant difference between the strains. Finally, to confirm the cellular localization of the protein Ndt1, spheroplasts of S. cerevisiae were subjected to confocal microscopy, which evidenced the co-location of Ndt1 protein with mitochondria in S. cerevisiae strain transformed with the construction pYES/ndt1. This same profile was not observed in strain ?ndt1?ndt2.
Preyat, Nicolas. "Tumor necrosis factor-induced necroptosis is regulated by nicotinamide adenine dinucleotide in a sirtuin-dependent manner". Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209470.
Pełny tekst źródłaOur findings indicate that NAD+ is protective against DNA damage-induced cell death and FAS-induced apoptosis, while, unexpectedly, it promotes TNF-induced necroptosis, a regulated form of necrosis. Indeed raising NAD+ cellular levels sensitized culture cells to necroptosis, while NAD+ depletion protected cells from this form of cell death. Furthermore, specific silencing of NAD+-dependent sirtuins was also found to be protective against TNF-induced necroptosis. Consistently, a pharmacological pan-sirtuin inhibitor called cambinol protected cells from necroptosis. Then, as necroptosis represents a back-up mechanism that may have evolved in response to viral pathogens expressing anti-apoptotic proteins, we demonstrated in an in vitro model mimicking viral infection that pharmacological sirtuin inhibition protected cells from poly I:C-induced necroptotic cell death. In vivo, we demonstrated that cambinol partially protected kidney from necrosis after ischemia/reperfusion. We have also shown that enhancing liver NAD+ concentration via isonicotinamide increases the susceptibility of mice to systemic inflammatory response syndrome (SIRS). Moreover, our preliminary data show that isonicotinamide substantially improves the ability of cyclophosphamide to trigger the rejection of the murine mastocytoma P815 tumor cell line.
Collectively, our observations point to a role for NAD+ in the control of necroptosis in a sirtuin-dependent manner. These observations may bear relevance to the better understanding of the pathophysiological consequences of excessive production of the pro-inflammatory cytokine TNF and the control of viral infections and tumor progression/immunotherapy. &
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
Smyth, Lisa M. "The nicotinamide adenine dinucleotide (NAD)/cyclic ADP-ribose/ADP-ribose system, new to the peripheral synapse". abstract and full text PDF (free order & download UNR users only), 2005. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3210943.
Pełny tekst źródłaBERTRAND, MARTINE. "Photoreduction du nicotinamide adenine dinucleotide phosphate par des etioplastes de haricot (phaseolus vulgaris l. Var commodore)". Paris 6, 1988. http://www.theses.fr/1988PA066079.
Pełny tekst źródłaBrunnbauer, Philipp [Verfasser]. "On the measurement and systemic relevance of extracellular nicotinamide adenine dinucleotide in human plasma / Philipp Brunnbauer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1206185988/34.
Pełny tekst źródłaSato, Yuichi. "Palmitate induces reactive oxygen species production and β-cell dysfunction by activating nicotinamide adenine dinucleotide phosphate oxidase through Src signaling". Kyoto University, 2014. http://hdl.handle.net/2433/188633.
Pełny tekst źródłaSheridan, Scott D. "Partial purification and characterization of F₄₂₀-dependent NADP reductase from Methanobrevibacter smithii strain DE1". PDXScholar, 1985. https://pdxscholar.library.pdx.edu/open_access_etds/3523.
Pełny tekst źródłaAli, Irshad. "Electrochemical investigations of the interactive behavior of Nicotinamide Adenine Dinucleotide (NAD+/NADH) with electrode surfaces: towards direct electrochemical regeneration of enzymatically-active NADH". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=117104.
Pełny tekst źródłaNicotinamide-adénine-dinucléotide NAD(H) est une coenzyme qui participe à un grand nombre de processus biochimiques dans lesquels elle agit comme une transporteuse d'électrons et d'atomes d'hydrogène. En dépit de sa forte utilisation potentielle dans l'industrie, son utilisation actuelle est très limitée à cause de son coût très élevé (en particulier celui du 1,4-NADH) et la nécessité d'être ajouté en quantités stœchiométriques dans les réacteurs biochimiques. Par conséquent, il est nécessaire de développer des méthodes de régénération in-situ du 1,4-NADH. Les méthodes électrochimiques sont d'un intérêt particulier en raison de leur coût potentiellement faible et l'isolement facile du produit. Cependant, le problème majeur dans la régénération électrochimique du 1,4-NADH est la formation d'un dimère enzymatiquement inactif, NAD2. Ce projet de doctorat est axé sur (i) l'étude des aspects fondamentaux de l'interaction du NAD+ avec la surface d'un électrode en carbone vitreux (GC), en termes de la cinétique de réduction et l'adsorption du NAD+ sur la surface du GC, et (ii) le développement d'électrodes pour la régénération électrocatalytique directe (non médiatisée) du composé 1,4-NADH, active enzymatiquement actif.Les mesures de polarisation potentiodynamique ont montré que dans les conditions expérimentales utilisées, la réaction de réduction du NAD+ est contrôlée par la diffusion. Cette irréversible (nécessite une surtension de plus de -550 mV) et est de pseudo premier ordre par rapport au NAD+. La cinétique de réduction du NAD+ sur GC, an potentiel formel du couple NAD +/NADH (-0.885 V), est lente, et modérément dépendante de la température. Le NAD+ est adsorbé sur la surface de l'électrode en GC. La cinétique d'adsorption du NAD+ s'est avérée dépendante de la charge surfacique. Le processus d'adsorption a été décrit par l'isotherme de Langmuir. L'énergie de Gibbs d'adsorption correspondante a montré que le processus d'adsorption est très spontané.L'influence du potentiel et du matériel de l'électrode sur la pureté du 1,4-NADH régénéré, a ensuite été étudiée. Il a été constaté que la régénération de 1,4-NADH à partir de NAD+, dans un réacteur électrochimique discontinu, employant des électrodes non modifiés est possible. La pureté (récupération) du 1,4-NADH régénéré sur ces électrodes a été jugée dépendante du potentiel et du matériel de l'électrode. L'origine de cette relationentre la nature elu nature ela matériel et le potentiel été liée à la force de liaison métal-hydrogène (M-Hads), et donc à la couverture du Hads sur la surface de l'électrode, que dépend du potentiel. Seuls les électrodes en GC et CNF ont été capables de produire la plus haute pureté du composé 1,4-NADH (99-100%), mais à des potentiels cathodiques le élevés (-2.3 V). Donc, pour produire 1,4-NADH de haute pureté à faibles potentiels cathodiques, la surface d'une électrode en GC a été modifiée par des nanoparticules (NPs) de platine et nickel, déposées par voie électrochimique. Il a été démontré que lorsque l'électrode en GC a été modifiées avec des NPs de Pt, le produit 1,4-NADH, avec une pureté de 100%, a été obtenu à -1.6 V, tandis que l'électrode en GC modifiée avec les NPs de Ni a produit 1,4-NADH avec une pureté de 100% déjà à -1.5 V. La haute pureté du 1,4-NADH formée sur les deux électrodes nano- modifiée a été prescrite à la formation des liaisons Pt-Hads et Ni-Hads à un potentiel nettement inférieur à celui sur une surface nue en GC. Il a été constaté que la pureté du 1,4-NADH régénérée sur les électrodes nano-modelées est dépendante du potentiel d'électrode, de la taille des nanoparticules et de leur couverture de la surfacique. Compte tenu de l'apport énergétique le coût de l'électrode, et le pourcentage de récupération du 1,4-NADH (i.e. sa pureté), l'électrode GC-Ni a été suggéré l'électrode de choix pour la régénération du 1,4-NADH parmi tous les électrodes étudiés (GC, CNF, Ti, Co, Cd, Ni, GC-Pt et GC-Ni).
Cao, Peter. "Age-related structural changes in the liver of old mice with SIRT1 overexpression in conjunction with NMN supplementation". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16872.
Pełny tekst źródłaBotta, Davide. "Strategies for structural studies of poly(ADP-ribose) glycohydrolase: Towards the validation of a novel therapeutic target". Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/145718.
Pełny tekst źródłaCoyle, Donna L. (Donna Lynn). "Modification of Cardiac Membrane Gsα by an Endogenous Arginine-Specific Mono-Adp-Ribosyltransferase". Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc332726/.
Pełny tekst źródłaPeters, Jeffery. "Effects of Nicotinamide Riboside and Beta-hydroxybutyrate on C. elegans Lifespan". Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/honors/531.
Pełny tekst źródłaWos, Melissa Louise, i n/a. "Methods For Understanding Bacterial Metabolic Activity In Activated Sludge". Griffith University. School of Environmental Engineering, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061031.151641.
Pełny tekst źródłaWos, Melissa Louise. "Methods For Understanding Bacterial Metabolic Activity In Activated Sludge". Thesis, Griffith University, 2005. http://hdl.handle.net/10072/367303.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Environmental Engineering
Full Text
Peres-Lascar, Audrey. "Etude des mécanismes moléculaires de la cross présentation antigénique dans les sous populations de cellules dendritiques conventionnelles murines". Paris 6, 2009. http://www.theses.fr/2009PA066095.
Pełny tekst źródłaSidhu, Navdeep Singh. "Crystal Structures of a Bacterial Isocitrate Dehydrogenase and the Human Sulfamidase". Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://hdl.handle.net/11858/00-1735-0000-0015-A383-5.
Pełny tekst źródłaFang, Lei. "Development and Characterization of an Iridium-Modified Electrochemical Biosensor for Potential Diabetic Patient Management". Cleveland, Ohio : Case Western Reserve University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1223049333.
Pełny tekst źródłaDepartment of Chemical Engineering Abstract Title from OhioLINK abstract screen (viewed on 10 April 2009) Available online via the OhioLINK ETD Center
Chaves, Izabel de Souza. "Efeitos fisiológicos da expressão reduzida de transportadores de NAD + em Arabidopsis thaliana". Universidade Federal de Viçosa, 2015. http://www.locus.ufv.br/handle/123456789/8357.
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Fundação de Amparo à Pesquisa do Estado de Minas Gerais
Nicotinamida adenina dinucleotídeo (NAD + ) e seu derivado NADP + são compostos essenciais em todos os organismos vivos e que estão envolvidos em transações energéticas, na sinalização celular e em diversas reações na forma de coenzimas. Alterações no catabolismo ou no anabolismo do NAD + podem modificar não apenas a sua concentração, mas também o poder redutor celular, impactando aspectos importantes do crescimento e desenvolvimento. Uma vez que as etapas finais da biossíntese de NAD + ocorrem no citosol, o mesmo precisa ultrapassar membranas biológicas para exercer suas funções dentro de organelas celulares. Neste trabalho, avaliou-se em Arabidopsis thaliana o papel dos transportadores cloroplastídico e mitocondrial de NAD + , denominados AtNDT1 e AtNDT2, respectivamente. Para tal, foram utilizadas linhagens mutantes obtidas por inserção do T-DNA e foram geradas plantas transgênicas contendo uma construção antisenso para os transportadores NDT1 e NDT2, sob o controle do promotor 35S, das quais, três linhagens com reduzida expressão de cada transportador foram selecionadas. Estas plantas foram caracterizadas extensivamente a nível fisiológico e bioquímico. Verificou-se que plantas com expressão reduzida de NDT1 apresentam maior número de folhas e área foliar específica em relação às plantas não transformadas (WT). Observaram-se também maiores taxas de fotossíntese por unidade de massa e, consequentemente, maior acúmulo de sacarose e amido em comparação com o WT. Entretanto, estas plantas apresentaram menor viabilidade do grão de pólen, redução no comprimento das síliquas e sementes abortadas. Já em plantas com reduzida expressão do transportador NDT2 descobriu-se que apesar de possuírem menor número de folhas, a área foliar aumentou. A fotossíntese nestas plantas diminuiu consideravelmente em decorrência de uma menor densidade estomática e condutância estomática. Concomitantemente, plantas com reduzida expressão de NDT2 apresentaram menor acúmulo de amido. A germinação das sementes e formação de plântulas foram menores e mais lentas em comparação com o WT. Além disso, houve aumento na concentração relativa de alguns ácidos graxos durante o estabelecimento das plântulas. Diante dos resultados obtidos, sugere-se que os transportadores de NAD + estão envolvidos na determinação do número de folhas e área foliar, na fotossíntese, na condutância estomática e nas concentrações de amido. Além disso, tecidos heterotróficos também são fortemente influenciados, especialmente aqueles envolvidos em processos reprodutivos. Para compreender a função deste transportador é necessário analisar não apenas a concentração celular dos nucleotídeos de pirimidina, mas também como alterações no status redox celular afetam o metabolismo vegetal. Assim, os dados obtidos neste trabalho sugerem que alterações no estado redox em cloroplastos e mitocôndrias causadas pela diminuição da expressão de NDT1 ou NDT2 afetam processos em outras organelas que não aquela em que ocorre a redução da expressão. Estes resultados abrem possibilidades para aplicações biotecnológicas, uma vez que a regulação da biossíntese e transporte de cofatores pode ser usada como uma ferramenta para estratégias de aumento da assimilação de carbono em plantas. Para tal, é necessário, no entanto compreender mais o papel destes transportadores em outros tecidos vegetais e condições adversas bem como o papel de enzimas chave que atuam no processo.
Nicotinamide adenine dinucleotide (NAD + ) and nicotinamide adenine dinucleotide phosphate (NADP + ) are indispensable redox-active components of all living organisms. These nucleotides play essential roles in signaling and in many reactions as they act as co-enzymes. NAD catabolism or anabolism changes impact not only the concentration of these coenzymes but also the cellular poise, modifying plant growth and development. Since the final steps of NAD + biosynthesis occurs in cytosol, this nucleotide needs to be imported by organelles to play its functions inside cellular organelles. This work analyzed the function of a plastid and a mitochondrial Arabidopsis thaliana NAD + transporter, named as AtNDT1 e AtNDT2 respectively. We have isolated T-DNA insertion mutants and three antisense lines, controlled by the 35S promoter, for NDT1 and NDT2. Plants with reduced expression of NDT1 and NDT2 were individually selected and characterized at physiological and biochemical level. It was verified that NDT1 low expression lines displayed higher leaf number and specific leaf area compared to wild type plants (WT). Interestingly, higher photosynthesis per mass unit and sucrose and starch concentration was observed. On the other hand, NDT1 low expression lines show less pollen viability and reduced silique length and increased the number of aborted seeds. The low expression NDT2 lines displayed reduced number of leaves and increased leaf area. Despite these phenotypes, the net photosynthetic rate decreased considerably due to lower stomatal conductance, possible as a consequence of lower stomatal density. Concomitantly, these plants showed lower starch accumulation during the day. The germination and seedling growth rate were reduced as compared to WT. Furthermore, the oil relative concentration increased during seedling establishment. Based on these results, we conclude that NAD + transporters have important function in determining leaf number, area, stomatal conductance, photosynthetic rate and starch accumulation. Moreover, heterotrophic tissues are strongly affected by the reduction in the expression of these transporters, especially those tissues involved in reproductive process. For a better understanding of the role played by these transporters, it is necessary to analyze not only nucleotide cellular concentration but also the redox poise in different cell compartments. Thus, the results presented in this thesis suggest that lower expression of NAD transporters alters redox poise in different organelles affecting important physiological processes. These results open possibilities for biotechnology application, once the regulation of biosynthesis and transport of cofactors might be used as a tool for increasing carbon assimilation in plants. Nonetheless, it is necessary understanding the role of these transporters in other plant tissues and plant cultivated under stress conditions involved in these processes.
Hentschke, Mike-Percy [Verfasser]. "Prüfung der parenteralen und enteralen Bioverfügbarkeit von reduziertem Nicotinamid-adenin-dinucleotid (NADH) im ZNS der narkotisierten Ratte mittels Laser-induzierter Fluoreszenzspektroskopie / Mike-Percy Hentschke". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024006859/34.
Pełny tekst źródłaPorpino, Suênia Karla Pacheco. "Nitrato orgânico 2-nitrato-1,3-dibutoxipropano (NDBP) atenua o estresse oxidativo e a hipertensão arterial mediada por angiotensina II via produção de óxido nítrico em animais experimentais". Universidade Federal da Paraíba, 2016. http://tede.biblioteca.ufpb.br:8080/handle/tede/9694.
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Background: Nitric oxide (NO) donors can act in the control and treatment of various cardiovascular complications, such as hypertension. In particular, an organic nitrate, 2-nitrate-1,3-dibutoxipropane (NDBP) developed in recent years by UFPB has shown great therapeutic potential. However, its mechanisms are not fully clarified. Aim: To investigate the effects and mechanisms of NDBP, elucidating their therapeutic potential in angiotensin II-mediated hypertension. Methods: In the first stage of the study, were performed in vitro experiments in normotensives Wistar rats (n=11) tissues for characterization of compound about ability to release NO by direct measurement of NO; and modulation of NADPH oxidase activity, by chemiluminescence technique. In the second stage of the study, in vivo experiments in C57BL / 6J mice (n=24), divided in four groups (control, NDBP, Ang II and Ang II + NDBP) were performed to investigate the therapeutic potential of NDBP in angiotensin II-mediated hypertension. The animals had implantation of osmotic minipumps containing Ang II (400 mg / kg / 24h) and after 9 days were treated with NDBP (40 mg / kg / day; ip). Blood pressure (BP) was measured by tail-cuff. At the end of the experiments, the animals were euthanized and blood and tissues were collected for analysis. Histopathological analyzes were performed using staining picrosirius. Superoxide levels were measured by NADPH oxidase activity via chemiluminescence and DHE fluorescence (5 mmol • L-1). Levels of serum nitrate/nitrite and cGMP were performed using specific kits. NADPH oxidase subunit expression were analyzed by real time qPCR. Putative antioxidant activity was determined by autoxidation with pyrogallol. Results: In vitro experiments revealed a dose-dependent increase in NO production mediated by NDBP in liver and kidney tissues, which was attenuated by the xanthine oxidase inhibitor febuxostat. In addition, the NDBP reduced NADPH oxidase activity and prevented its activation induced by ANG II. In vivo experiments showed that NDBP prevents the increase in hypertension in mice with chronic infusion of ANG II. This results were associated to the attenuation of cardiac hypertrophy, renal fibrosis, and reduced NADPH oxidase-derived oxidative stress in the kidneys, the heart, and liver. Furthermore, NDBP also increased plasma levels of nitrite and nitrate. On the other hand, the autoxidation with pyrogallol revealed that NDBP does not act as a direct antioxidant, justifying its involvement in the modulation of NADPH oxidase. Conclusions: The organic nitrate NDBP prevents the progression of angiotensin II-mediated hypertension. Regarding the mechanisms, our findings suggest that NDBP treatment is associated with sustained NO release and attenuated activity of NADPH oxidase, which requires functional xanthine oxidase.
Introdução: Doadores de óxido nítrico (NO) podem atuar no controle e tratamento de diversas complicações cardiovasculares, como por exemplo, a hipertensão arterial. Em particular, um nitrato orgânico, 2-nitrato-1,3-dibutoxipropano (NDBP) desenvolvido nos últimos anos pela UFPB vem apresentando grande potencial terapêutico. No entanto, seus mecanismos não estão totalmente esclarecidos. Objetivo: Investigar os efeitos e os mecanismos de ação do NDBP, elucidando seu potencial terapêutico na hipertensão arterial induzida por Angiotensina II (ANG II). Métodos: Na primeira etapa do estudo foram realizados experimentos in vitro em tecidos de ratos Wistar normotensos (n=11) para caracterização do composto, sobre sua capacidade de liberação de NO, por meio da medida direta de NO; e modulação da atividade da enzima NADPH oxidase, pela técnica de quimioluminescência. Na segunda etapa do estudo, experimentos in vivo em camundongos C57BL/6J (n=24), classificados em quatro grupos (Controle, NDBP, ANG II e ANG II + NDBP), foram realizados para investigar o potencial terapêutico do NDBP na hipertensão induzida por ANG II. Os animais tiveram implante de minibombas osmóticas contendo ANG II (400 μg/kg/24h) e após 9 dias receberam tratamento com NDBP (40 mg/kg/dia; i.p.). A pressão arterial (PA) foi verificada via pletismografia de cauda. Ao término dos experimentos, os animais foram eutanasiados e tecidos e sangue foram coletadas para análise posterior. Análises histopatológicas foram realizadas utilizando a coloração com Picro-sirius. Os níveis de superóxido foram mensurados por meio da atividade da enzima NADPH oxidase, via quimioluminescência e fluorescência com DHE (5 mmol·L−1). Além disso, os níveis séricos de nitrato/nitrito e cGMP foram realizados, utilizando kits específicos. Foi investigada também a expressão de subunidades da enzima NADPH oxidase pela técnica de qPCR em tempo real e a possível atividade antioxidante por meio da autoxidação com pyrogallol. Resultados: os experimentos in vitro utilizando tecidos de fígado e rim revelaram um aumento dose-dependente na produção de NO, mediado pelo NDBP, que foi atenuado pelo inibidor da enxima xantina oxidase, o febuxostato. Além disso, o NDBP reduziu a atividade da NADPH oxidase e preveniu sua ativação induzida pela ANG II. Os experimentos in vivo mostraram que o NDBP previne o aumento da hipertensão arterial em camundongos com infusão crônica de ANG II. Esses resultados foram associados à atenuação da hipertrofia cardíaca, fibrose renal, e redução do estresse oxidativo mediado pela redução da atividade da enzima NADPH oxidase nos rins, coração e fígado. Além disso, o NDBP aumentou os níveis plasmáticos de nitrito e nitrato. Por outro lado, a autooxidação com pyrogalol revelou que o NDBP não atua como um antioxidante direto, justificando então sua participação na modulação da NADPH oxidase. Conclusão: o nitrato orgânico NDBP impede a progressão da hipertensão arterial mediada pela angiotensina II. Em relação aos seus mecanismos, os achados sugerem que o tratamento com NDBP está associado a uma contínua liberação de NO e redução da atividade da enzima NADPH oxidase, que parece ser dependente da xantina oxidase funcional.
Noriega, Esteban Núria. "The Rtg1 and Rtg3 proteins are novel transcription factors regulated by the yeast hog1 mapk upon osmotic stress". Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7158.
Pełny tekst źródłaIn Saccharomyces cerevisiae the adaptation to high osmolarity is mediated by the HOG (high-osmolarity glycerol) pathway, which elicits different cellular responses required for cell survival upon osmostress. Regulation of gene expression is a major adaptative response required for cell survival in response to osmotic stress. At least five transcription factors have been reported to be controlled by the Hog1 MAPK. However, they cannot account for the regulation of all of the genes under the control of the Hog1 MAPK. Here we show that the Rtg1/3 transcriptional complex regulates the expression of specific genes upon osmostress in a Hog1-dependent manner. Hog1 phosphorylates both Rtg1 and Rtg3 proteins. However, none of these phosphorylations are essential for the transcriptional regulation upon osmostress. Here we also show that the deletion of RTG proteins leads to osmosensitivity at high osmolarity, suggesting that the RTG-pathway integrity is essential for cell survival upon stress.
Vendrell, Arasa Alexandre. "SCF cdc4 regulates msn2 and msn4 dependent gene expression to counteract hog1 induced lethality". Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7153.
Pełny tekst źródłaTambé hem observat que la mort cel·lular causada per l'activació sostinguda de Hog1 és deguda a una inducció d'apoptosi. L'apoptosi induïda per Hog1 és inhibida per la mutació al complexe SCFCDC4. Per tant, la via d'extensió de la vida és capaç de prevenir l'apoptosi a través d'un mecanisme desconegut.
Sustained Hog1 activation leads to an inhibition of cell growth. In this work, we have observed that the lethal phenotype caused by sustained Hog1 activation is prevented by SCFCDC4 mutants. The prevention of Hog1-induced cell death by SCFCDC4 mutation depends on the lifespan extension pathway. Upon sustained Hog1 activation, SCFCDC4 mutation increases Msn2 and Msn4 dependent gene expression that leads to a PNC1 overexpression and a Sir2 deacetylase hyperactivation. Then, hyperactivation of Sir2 is able to prevent cell death caused by sustained Hog1 activation.
We have also observed that cell death upon sustained Hog1 activation is due to an induction of apoptosis. The apoptosis induced by Hog1 is decreased by SCFCDC4 mutation. Therefore, lifespan extension pathway is able to prevent apoptosis by an unknown mechanism.
Tompson-Mennitz, A. "A pilot longitudinal examination of biomarkers and social cognition in Multiple Sclerosis". Thesis, 2022. https://eprints.utas.edu.au/47642/.
Pełny tekst źródłaChen, meiyau, i 陳媺媱. "Nicotinamide Adenine Dinucleotide Plays A Crucial Role In Calorie Restriction Extended Replicative Lifespan Of Human Hs68 Cells". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/97047196245229528678.
Pełny tekst źródła中州科技大學
保健食品系
100
Caloric restriction (CR) can extend the lifespan of organisms. Nicotinamide adenine dinucleotide (NAD+) is one of bioactive from of vitamin B3. Sirtuins is a protein family called NAD+-dependent deacetylase, which is considered as a longevity protein. FK866 is an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which is the rate limiting enzyme in the salvage pathway of NAD+ synthesis from nicotinamide and has ability to decrease intracellular NAD+ level. In this study, we examined whether CR can increase intracellular NAD+ levels, and then activate SIRT1 and extend replicative lifespan of human Hs68 cells. Using cells cultured at lower levels of glucose than normal level of glucose in medium (glucose restriction; GR) to mimic CR, we compared the effects of GR, NAD+ and FK866 on cell lifespan, intracellular NAD+ levels, SIRT1 activity and senescence associated -galactosidase (SA-G) activity. We also examined whether the effects of FK866 on Hs68 cells can be antagonized by GR and adding NAD+ into the culture medium. The lifespan of cells was measured as the cumulated growth curve of population doubling levels. The biomarker of cell senescence was detected by determination of senescence associated -galactosidase (SA-G) activity using X-Gal staining. Intracellular NAD+ was determined by an acid extraction method and followed by an enzymatic cycling method. SIRT1 activities were determined by SIRT1 Direct Fluorescent Screening Assay Kit or used p53 acetylation to represent cellular activities of SIRT1. The results showed that GR (>5day) could significantly increase NAD+ levels in cells, activated SIRT1 activity, and extended the lifespan of Hs68 cells. Add NAD+ in to the medium showed with similar effects as GR. Oppositely, FK866 has abilities to reduce intracellular NAD+ levels, shorten the cells lifespan, decrease SIRT1 activity, and increase SA-βG activity. Importantly, all of these effects of FK866 on Hs68 cells can be effectively blocked by GR or adding NAD+ into the medium. The results demonstrated that increase of intracellular NAD+ level plays a crucial role in the mechanism of CR-extended lifespan of human Hs68 cells.
Weeks, Martha Lee. "Design of a reagentless enzymatic amperometric alcohol biosensor yeast alcohol dehydrogenase and nicotinamide adenine dinucleotide on vertically aligned carbon nanofibers /". 2006. http://etd.utk.edu/2006/WeeksMartha.pdf.
Pełny tekst źródłaTamsett, Thomas J. "Sodium activated potassium channels (K(Na)) are modulated by nicotinamide adenine dinucleotide (NAD+) in adult dorsal root ganglion (DRG) neurons". 2008. http://proquest.umi.com/pqdweb?did=1588771761&sid=17&Fmt=2&clientId=39334&RQT=309&VName=PQD.
Pełny tekst źródłaTitle from PDF title page (viewed on Feb. 12, 2009) Available through UMI ProQuest Digital Dissertations. Thesis adviser: Bhattacharjee, Arin, Slaughter, Malcolm Includes bibliographical references.
Guo, Han Wen, i 郭瀚文. "Detection of Metabolic Changes during Osteogenic Differentiation of Human Mesenchymal Stem Cells by Fluorescence Lifetime Changes of Reduced Nicotinamide Adenine Dinucleotide (NADH)". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/49539012464348170065.
Pełny tekst źródła國立陽明大學
生醫光電工程研究所
96
Stem cells have been demonstrated having potential applications in tissue engineering and regenerative medicine. One of the known metabolic properties of stem cell is the change of metabolic switch from stem cells to differential state. The metabolic shift is form anaerobic glycolysis to the more efficient mitochondrial oxidative metabolism. Base on this property of stem cell, we observed the lifetime of reduced nicotinamide adenine dinucleotide (NADH) via two-photon Fluorescence lifetime imaging microscopy (FLIM) during osteogenic differentiation of human mesenchymal stem cells (hMSCs), to replace many of these methods are invasive that damage cell or need pre-labeling. In our study, we investigated that NADH lifetime increased from ~1000 ps to ~1200 ps and the free-/bound- protein ratio of NADH decreased from~3.0 to ~2.1 during the osteogenic differentiation of hMSCs. Then we treated different metabolic inhibitors into fiberblasts(CCD) and measured NADH lifetime. After treating different inhibitors 24 hr, NADH lifetime only increased to ~1200 ps in the treatment of oligomycin A. In the short terms (2 hr), NADH lifetime after treating KCN decreased to ~700 ps initially, and then increased to ~1000 ps after 1 hr, which is almost the same with control. Other inhibitors didn’t influence the change of NADH lifetime in the short terms. These result is very different from our hypothesis. In MSCs, we considered the increase of NADH lifetime resulted from Complex number of OXPHOS system increased. However, in treatment of metabolic inhibitors, cells not only changed in metabolism but also the cellular condition became very complicated. Our results suggest that detecting NADH lifetime by FLIM has potential to observe the metabolic change during the osteogenic differentiation of hMSCs. But we need more researches to understand the complicated condition resulted from the treatment of metabolic inhibitors in the measurement of NADH lifetime.