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Relevant bibliographies by topics / Pyridine nucleotides

Academic literature on the topic 'Pyridine nucleotides'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 January 2023

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Journal articles on the topic "Pyridine nucleotides":

1

Abdellatif, Maha. "Sirtuins and Pyridine Nucleotides." Circulation Research 111, no. 5 (August 17, 2012): 642–56. http://dx.doi.org/10.1161/circresaha.111.246546.

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2

COSNIER, S., and K. LELOUS. "Amperometric detection of pyridine nucleotides via immobilized viologen-accepting pyridine nucleotide oxidoreductase or immobilized diaphorase." Talanta 43, no. 3 (March 1996): 331–37. http://dx.doi.org/10.1016/0039-9140(95)01755-0.

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3

O'Reilly, T., and D. F. Niven. "Pyridine nucleotide metabolism by extracts derived from Haemophilus parasuis and H. pleuropneumoniae." Canadian Journal of Microbiology 32, no. 9 (September 1, 1986): 733–37. http://dx.doi.org/10.1139/m86-133.

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A variety of biologically important pyridine nucleotides and precursors were examined for their capacities to serve as substrates for the synthesis of NAD by cell fractions derived from Haemophilus parasuis and H. pleuropneumoniae. Of the compounds tested, only NMN and nicotinamide riboside were converted to NAD. These reactions required ATP as co-substrate, and fractions from both organisms could also catalyze the ATP-dependent synthesis of NADP from NAD. In the absence of ATP, and depending on the pyridine compound under study, NAD, NMN, nicotinamide riboside, and also nicotinamide, were detected as products of catabolisra. It is concluded that these haemophili possess either three-membered pyridine nucleotide cycles or two-membered cycles with synthetic branches originating with nicotinamide riboside. It is also possible that the pyridine nucleotide cycles of both organisms have nonrecycling branches resulting in the "waste" of usable pyridine compound in the form of nicotinamide.

4

Richter, C., and P. Meier. "Inhibition of pro-oxidant-induced mitochondrial pyridine nucleotide hydrolysis and calcium release by 4-hydroxynonenal." Biochemical Journal 269, no. 3 (August 1, 1990): 735–37. http://dx.doi.org/10.1042/bj2690735.

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Intra- and extra-mitochondrial Ca2+ participates in vital cellular processes. This work investigates the influence of 4-hydroxynonenal (HNE) on pro-oxidant-induced Ca2+ release from rat liver mitochondria. Ca2+ movements across the mitochondrial inner membrane, the pyridine nucleotide redox state and pyridine (nicotinamide) nucleotide hydrolysis were analysed. HNE did not influence Ca2+ uptake by mitochondria, but inhibited in a concentration-dependent manner Ca2+ release induced by t-butylhydroperoxide (tbh). Total inhibition was achieved with about 50 microM-HNE. Ca2+ release induced by the pro-oxidant alloxan was also inhibited by HNE. Oxidation of pyridine nucleotides, induced by tbh through the concerted action of glutathione peroxidase, glutathione reductase and the energy-linked transhydrogenase, was not affected by up to 50 microM-HNE. In contrast, HNE inhibited pyridine nucleotide hydrolysis in a concentration-dependent manner. The data suggest that HNE toxicity may be in part attributed to an impaired intramitochondrial Ca2+ homeostasis.

5

Billington, Richard A., Santina Bruzzone, Antonio De Flora, Armando A. Genazzani, Friedrich Koch-Nolte, Mathias Ziegler, and Elena Zocchi. "Emerging Functions of Extracellular Pyridine Nucleotides." Molecular Medicine 12, no. 11-12 (November 2006): 324–27. http://dx.doi.org/10.2119/2006-00075.billington.

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6

Nakamura, Michinari, Aruni Bhatnagar, and Junichi Sadoshima. "Overview of Pyridine Nucleotides Review Series." Circulation Research 111, no. 5 (August 17, 2012): 604–10. http://dx.doi.org/10.1161/circresaha.111.247924.

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7

Janero, D. R., D. Hreniuk, H. M. Sharif, and K. C. Prout. "Hydroperoxide-induced oxidative stress alters pyridine nucleotide metabolism in neonatal heart muscle cells." American Journal of Physiology-Cell Physiology 264, no. 6 (June 1, 1993): C1401—C1410. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1401.

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An oxidant burden established by hydrogen peroxide (H2O2) overload may elicit postischemic myocardial damage. We assess herein the influence of H2O2-induced oxidative stress on heart muscle pyridine nucleotide metabolism. Exposure of neonatal rat cardiomyocytes to 50 microM-1.0 mM H2O2 bolus rapidly shifted their pyridine-nucleotide redox balance toward oxidation. At least 30% of the observed NADPH oxidation was independent of glutathione cycle activity and appeared chemical in nature with H2O2 itself, and not a radical metabolite, acting as oxidant. Cell exposure to H2O2 also depleted cardiomyocyte pyridine nucleotides as a consequence of enhanced utilization. The oxidative stress activated one major route of pyridine nucleotide catabolism (i.e., protein ADP-ribosylation) without acute inhibitory effect upon the other (cleavage by NAD glycohydrolase). The limited NAD sparing by metal chelators and inhibitors of ADP-ribosylation reflected pyridine nucleotide utilization for repair of single-strand DNA breaks caused by hydroxyl-like radicals formed intracellularly through iron-dependent H2O2 reduction. Cardiomyocyte NAD depletion during H2O2-induced oxidative stress was independent of cell integrity and lipid peroxidation. The NAD lost after a discrete H2O2 "pulse" was only partly replenished over a 24-h postinjury period. These data demonstrate that cardiomyocyte pyridine nucleotide metabolism is a nonperoxidative injury target that is chronically affected by H2O2 overload. Derangement of myocardial pyridine nucleotide pools due to oxidative stress may contribute to ischemic heart injury in vivo by interfering with cardiac hydrogen metabolism and redox balance.

8

Beslin, A., M. P. Vié, J. P. Blondeau, and J. Francon. "Identification by photoaffinity labelling of a pyridine nucleotide-dependent tri-iodothyronine-binding protein in the cytosol of cultured astroglial cells." Biochemical Journal 305, no. 3 (February 1, 1995): 729–37. http://dx.doi.org/10.1042/bj3050729.

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High-affinity 3,3′,5-tri-iodo-L-thyronine (T3) binding (Kd approximately 0.3 nM) to the cytosol of cultured rat astroglial cells was strongly activated in the presence of pyridine nucleotides. A 35 kDa pyridine nucleotide-dependent T3-binding polypeptide (35K-TBP) was photoaffinity labelled using underivatized [125I]T3 in the presence of pyridine nucleotides and the free-radical scavenger dithiothreitol. Maximum activations of T3 binding and 35K-TBP photolabelling were obtained at approx. 1 x 10(-7) M NADP+ or NADPH, or 1 x 10(-4) M NADH. NAD+ and other nucleotides were without effect. NADPH is the form which activates T3 binding and 35K-TBP photolabelling, since cytosol contains NADP(+)-reducing activity, and the activation of both processes in the presence of NADPH and NADP+ was prevented by an exogenous NADPH oxidation system. NADPH behaved as an allosteric activator of T3 binding. The NADPH oxidation system promoted the release of bound T3 in the absence of any change in the total concentration of the hormone. The 35K-TBP photolabelling and [125I]T3 binding were similarly inhibited by non-radioactive T3 (half-maximum effect at 0.5-1.0 nM T3). The concentrations of iodothyronine analogues that inhibited both processes were correlated (3,3′,5-tri-iodo-D-thyronine > or = T3 > L-thyroxine > tri-iodothyroacetic acid > 3,3′5′-tri-iodo-L-thyronine). Molecular sieving and density-gradient centrifugation of cytosol identified a 65 kDa T3-binding entity, which included the 35K-TBP. These results indicate that 35K-TBP is the cytosolic entity involved in the pyridine nucleotide-dependent T3 binding, and suggest that the sequestration and release of intracellular thyroid hormones are regulated by the redox state of astroglial cell compartment(s).

9

Buillard, C., and J. L. Dreyer. "Inhibition of CA2+Efflux by Pyridine Nucleotides." Journal of Receptor Research 11, no. 1-4 (January 1991): 653–63. http://dx.doi.org/10.3109/10799899109066433.

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10

Liu, Man, Shamarendra Sanyal, Ge Gao, Iman S. Gurung, Xiaodong Zhu, Georgia Gaconnet, Laurie J. Kerchner, et al. "Cardiac Na + Current Regulation by Pyridine Nucleotides." Circulation Research 105, no. 8 (October 9, 2009): 737–45. http://dx.doi.org/10.1161/circresaha.109.197277.

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Dissertations / Theses on the topic "Pyridine nucleotides":

1

O'Reilly, Michael Terrence Stewart. "Pyridine nucleotide metabolism by porcine haemophili." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=73973.

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2

Graham, François. "Regulation of 5-oxo-ETE synthesis by pyridine nucleotides in aging neutrophils." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116087.

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Neutrophils (polymorphonuclear leukocytes) are short lived granulocytes that playa primordial role in host innate defense against invading pathogens. Freshly isolated neutrophils spontaneously undergo apoptosis when cultured, which is associated with oxidative stress. We found that there is a dramatic shift in the metabolism of the 5-lipoxygenase product 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) from its biologically inactive o-oxidation product in freshly isolated neutrophils to the potent granulocyte chemoattractant 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE) in neutrophils cultured for 24 h. o-oxidation of the chemoattractant leukotriene B4 (LTB4) was also reduced in aging neutrophils incubated with arachidonic acid, resulting in higher levels of LTB4. The reduced o-oxidation activity appeared to be due to a decrease in active LTB4 20-hydroxylase. In contrast, the increased 5-oxo-ETE formation was not associated with an increase in the amount of active 5-hydroxyeicosanoid dehydrogenase, which is required for its formation, but rather with a dramatic increase in its cofactor NADP +. NAD+ levels also increased, but NADPH levels remained unchanged after 24 h. There was also evidence for increased oxidative stress (high GSSG/GSH) in aging neutrophils. The changes in 5-HETE metabolism and pyridine nucleotides in cultured neutrophils could be inhibited by neutrophil survival factors and antioxidants. These results suggest that in severe inflammation, aging neutrophils that have evaded rapid uptake by macrophages may produce increased amounts of the chemoattractants 5-oxo-ETE and LTB4, resulting in delayed resolution of inflammation. Similarly, we found that the NADPH oxidase activator PMA caused a very rapid and dramatic increase in NADP + levels in both freshly isolated and cultured neutrophils, accompanied by a rapid increase in 5-oxo-ETE synthesis and reduced o-oxidation activity. Surprisingly, this was not accompanied by a corresponding decline in NADPH levels, which instead initially increased, but rather by a precipitous reduction in NAD+, which mirrored the increase in NADP+. These results suggest that the phosphorylation of NAD+ by NAD kinase may be very important for providing both NADP+ for 5-oxo-ETE synthesis and NADPH for the respiratory burst.

3

Kirvelaitytė, Dovilė. "Hipertermijos poveikis adenino ir piridino nukleotidų koncentracijai kepenų ląstelėse ir audinyje." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2010. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2010~D_20100614_095031-16530.

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Šilumos taikymas įvairioms ligoms gydyti jau buvo naudojamas senovės Egipto, Graikijos, Romos civilizacijose daugiau kaip prieš 2000 m. pr. Šiuo metu hipertermija plačiai taikoma visame pasaulyje gydant vėžį, nes tai pigus ir patogus metodas turintis mažą šalutinį poveikį. Mokslininkai nustatė, kad vėžinės ląstelės greičiau žūsta esant aukštesnei už fiziologinę (41-45°C) temperatūrai, todėl hipertermija, derinama su kitais vėžio gydymo metodais (radioterapija, chemoterapija, imunoterapija ir chirurgija), tampa efektyvesniu metodu. Kadangi yra mažai žinoma apie hipertermijos poveikio mechanizmą sveiko audinio ląstelėms karščiavimo, hiperterminio vėžio gydymo ar gydymo termoabliacija metu, todėl yra svarbu nustatyti hipertermijos paveiktų ląstelių gyvybingumą bei hipertermijos poveikį adenino ir piridino nukleotidų koncentracijoms. Šio darbo tikslas buvo įvertinti hipertermijos, būdingos nutolusioms nuo termozondo audinio sritims poveikį, adenino ir piridino nukleotidų koncentracijoms žiurkės kepenų ląstelėse bei audinyje. Buvo naudojamas jonų porų efektyviosios skysčių chromatografijos metodas, leidžiantis vienoje chromatografinėje analizėje išskirstyti labai skirtingo hidrofobiškumo junginius. Taip pat buvo vertintas gyvų ir negyvų ląstelių skaičius gautoje hepatocitų suspensijoje panaudojant tripano mėlio metodą bei NAD(P)H fluorescencijos pokyčiai kepenų audinyje termoabliacijos metu. Gauti rezultatai parodė, kad išskirti hepatocitai pasižymėjo dideliu gyvybingumu (8... [toliau žr. visą tekstą]
The application of heat in the treatment of disease was first recorded in the ancient civilizations of Egypt, Greece, and Rome from as early as 2000 BC. Nowadays hiperthermia is widely using in cancer diseases in all the world. It was determined by many scientists that cancer cells are more sensitive for supraphysiological temperature (41-45°C) killing compared to normal cells. There are numerous evidences that hyperthermia can increase the effectiveness of other cancer therapies: radiotherapy, chemotherapy, immunotherapy and surgery. There is little known about the mechanisms of hyperthermia effects on healthy tissue, which are important in fever, in hyperthermic treatment of neighboring tumour and in thermoablation. Therefore it is very important to determinate the vability of cells during different hyperthermic treatment and hyperthermic effects of adenine ir pyridine nucleotides concentrations.The aim of study was to value the effect of hyperthermia,which is typical remote from thermoprobe tissue areas, on the concentration of adenine and pyridine nucleotides in hepatocytes and liver tissue. It was used ion-pair high-performance liquid chromatography method, which allows to disperse different combinations of hydrophobicity. Also were evaluated live and dead cells quantity in the suspension through tripan blue method and NAD(P)H fluorescence changes in liver tissue during the ablation. The results showed that isolated hepatocytes exhibited with high viability (80%)... [to full text]

4

Djerada, Zoubir. "Récepteurs P2Y et Cardioprotection : implication du récepteur P2Y11-like dans le préconditionnement pharmacologique induit par le NAADP extracellulaire." Thesis, Reims, 2013. http://www.theses.fr/2013REIMM201.

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L’infarctus du myocarde (IC) représente plus de 15 % de la mortalité mondiale liés aux maladies cardiovasculaires (MC). En absence d’une rapide reperfusion des coronaires occluses, aucune intervention thérapeutique n’est capable de limiter les effets délétères de l’IC. Un des moyens les plus efficaces de la cardioprotection, étudié en recherche, est le préconditionnement cardiaque ischémique (PCI). L’adénosine libérée au cours du PCI active via ces récepteurs P1 les voies de cardioprotection. Des études mettent en évidence également l’implication des purinorécepteurs P2Y dans la cardioprotection. Les récepteurs P2Y2, 4 et 6 sont les plus étudiés dans la cardioprotection. Les récepteurs P2Y sont sensibles aux nucléotides comme l’ATP et l’UTP libérés au cours de l’ischémie. Parmi les récepteurs P2Y seul le récepteur P2Y11 est doublement couplé à l’adénylate cyclase et à la phospholipase C (PLC). Il est également le seul récepteur dont le polymorphisme génétique, induisant une perte du signal métabotropique, prédispose à plus de risques d’IC et d’inflammation dans toutes les catégories d’âge indépendamment des facteurs de risques variables de l’IC (Amisten et al., 2007). Ceci suggère un important rôle du récepteur P2Y11 dans la prévention primaire et comme cible thérapeutique de l’infarctus du myocarde. Le β-NAD, nucléotide à base de pyridine, est libéré au cours de l’ischémie comme les médiateurs de cardioprotection notamment l’adénosine, l’ATP et l’UTP. Cependant, aucune étude ne s’est intéressée spécifiquement aux rôles du P2Y11 et des nucléotides pyridiniques, comme médiateurs, dans la cardioportection alors que le NAADP, un métabolite du β-NAD, est rapporté comme agoniste (Moreschi et al., 2008) du récepteur P2Y11. Dans ce travail, nous avons mis en évidence pour la première fois l’augmentation des concentrations interstitielles des métabolites du β-NAD comme le NAADP au cours de l’ischémie. L’augmentation des concentrations du NAADP décrit une cinétique comparable à celle de l’adénosine. Le NAADP extracellulaire ([NAADP]e), appliqué avant un cycle d’ischémie/reperfusion (I/R), déclenche une cardioprotection envers les effets délétères de l’I/R. En effet, le [NAADP]e améliore les fonctions contractiles, réduit les contractures, les arythmies de reperfusion et la taille de l’infarctus, dans un modèle d’I/R cardiaque chez le rat. Ce préconditionnement pharmacologique induit par le [NAADP]e implique les récepteurs P2Y11-like. Dans un modèle de cardiomyocytes, nous mettons en évidence l’activité métabotropique spécifique du récepteur P2Y11-like déclenché par le [NAADP]e. Le [NAADP]e déclenche via le récepteur P2Y11-like l’activation de la PKCε, ERK1/2, AKT et GSK-3β, des protéines kinases de prosurvie cellulaire, ce qui explique ses effets cardioprotecteurs. La phosphorylation des protéines de prosurvie cellulaire nécessite la médiation de la PKA, de la PLC et de la src. Le NF546, un nouvel agoniste sélectif du récepteur P2Y11, déclenche une activité métabotropique semblable à celle du [NAADP]e, confirmant ainsi l’existence fonctionnelle du récepteur P2Y11-like au niveau des cardiomyocytes de rat. L’activation du récepteur P2Y11-like, que ce soit par le [NAADP]e ou le NF546, induit une augmentation des concentrations intracellulaires du β-NAD et de ses métabolites, le NADP, le NAADP, le NAAD et l’ADP ribose cyclique. Le β-NAD, le NAADP comme le NAAD, ont été impliqués dans le déclenchement au niveau intracellulaire des voies de cardioprotection comme la voie des sirtuines et de l’autophagie. Ces mécanismes peuvent être complementaires de l’effet cardioprotecteur du [NAADP]e. L’ensemble de nos données conforte le rôle cardioprotecteur du récépteur P2Y11 et suggère que le NAADP interstitiel accumulé au cours de l’ischémie pourrait avoir un rôle de facteur paracrine de survie cellulaire améliorant la survie des cardiomyocytes au cours des évènements ischémiques
Myocardial infarction (MI) accounts for more than 15 % of global deaths related to cardiovascular diseases (CD). In the absence of a prompt reperfusion of occluded coronary arteries, none of therapeutic interventions is able to limit the deleterious effects of MI. One of the most effective means of cardioprotection, studied in research, is the ischemic cardiac preconditioning (ICP). Adenosine released during ICP triggers, via P1 receptors, cardioprotective effects. Involvement of the purinoceptors (P2Y) in cardioprotective effects has been also reported. P2Y2,4,6 receptors, the most studied P2Y receptors in cardioprotection, are activated by the nucleotides released during ischemia such as ATP and UTP. Among the P2Y receptors, P2Y11 is dually coupled to Gs and Gq proteins and is the single P2Y receptor which has been linked, via a genetic polymorphism, to an increased risk of acute myocardial infarction and elevated levels of C-reactive protein in humans in all age groups (Amisten et al., 2007). This suggests for the P2Y11 receptor an important role in primary prevention and as a therapeutic target of the P2Y11 receptor for myocardial infarction. β-NAD, a pyridine nucleotide, is released during ischemia like adenosine, ATP and UTP. However, no study has focused on the roles of P2Y11 receptor and pyridine nucleotide in mediating cardioprotective effects while NAADP, a β-NAD metabolite, has been reported as an agonist (Moreschi et al., 2008) of the P2Y11 receptor. In this work, we show, for the first time, increased interstitial concentrations of NAADP during ischemia. Interstitial kinetics of NAADP is similar to adenosine. Using a pharmacological preconditioning protocol, triggered by extracellular NAADP ([NAADP]e) before a prolonged ischemia/reperfusion (I/R), rat hearts rapidly recovered post-ischemic contractile function and displayed attenuated contracture, infarct size and arrhythmogenesis. This pharmacological preconditioning involves the P2Y11-like receptor. In cardiomyocytes culture, [NAADP]e induces specific metabotropic response of the P2Y11-like receptor. [NAADP]e triggers via the P2Y11-like receptor prosurvival protein kinases activation such as PKCε, ERK1/2, AKT and GSK-3β which explains its protective effects. Phosphorylation of prosurvival protein kinases requires the mediation of PKA, PLC and src. As with [NAADP]e, the NF546, a new selective agonist of P2Y11 receptor, triggers a metabotropic activity, thus confirming the functional existence of P2Y11-like receptor in rat cardiomyocytes. Activation of the P2Y11-like receptor, either by [NAADP]e or NF546 induced an increase in intracellular concentrations of β-NAD and its metabolites, NADP, NAADP, NAAD and cyclic ADP ribose. More, β-NAD, NAADP as well as NAAD have been involved in activation of cardioprotective pathways such as sirtuine pathways and autophagy. Taken together, our data demonstrate for the first time that the P2Y11 receptor mediates cardioprotective effects induced by [NAADP]e. NAADP is released during ischemia suggesting that [NAADP]e may act as a paracrine survival factor, prolonging cardiomyocytes lifespan during ischemic events

5

Buckley, Patrick Anthony. "Structural studies on pyridine nucleotide dependent enzymes." Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392543.

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6

Wilson, Heather Louise. "Regulation of calcium mobilisation by pyridine nucleotide metabolites." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298417.

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7

Boonstra, Birgitte. "A study of bacterial soluble pyridine nucleotide transhydrogenases." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621214.

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8

Denicola-Seoane, Ana. "Studies on pyridine nucleotide-dependent processes in Haemophilus influenzae." Diss., Virginia Polytechnic Institute and State University, 1989. http://hdl.handle.net/10919/54514.

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Haemophilus influenzae and related species have a unique requirement for externally-provided NAD; therefore, several pyridine nucleotide-requiring enzymes become important for the survival of these pathogens. Haemophilus influenzae ATP:NMN adenylyltransferase was partially purified 15-fold with a 27% yield using dye affinity chromatography. Affinity chromatography was also used to purify NAD kinase from Haemophilus influenzae, 18-fold with a 32% yield. Substrate specificity studies of these enzymes demonstrated the enzymes to function with 3-acetylpyridine analogs of their respective substrates. A membrane-bound NMN glycohydrolase was demonstrated in Haemophilus influenzae. The enzyme functions with 3-acetylpyridine mononucleotide as a substrate, and is inhibited effectively by 3-aminopyridine mononucleotide. The possible involvement of this enzyme in the transport of NMN into the cytoplasm is discussed Growth inhibition studies demonstrated that 3-aminopyridine mononucleotide is a potent inhibitor of growth of the organism and could inhibit growth by inhibiting the transport of NMN. The previously reported inhibition of growth by the 3-aminopyridine adenine dinucleotide was attributed to the formation of the mononucleotide through the reaction catalyzed by the Haemophilus influenzae periplasmic nucleotide pyrophosphatase. A cytosolic lactate dehydrogenase, specific for D(-)-lactate was purified to electrophoretic homogeneity 2100-fold with a 14% yield. The purified enzyme was demonstrated to be a tetramer of M, = 135,000. It catalyzes essentially the reduction of pyruvate with very low activity observed for the oxidation of D(-)-lactate. An optimum pH of 7.2 was determined for the reduction of pyruvate with NADH as the coenzyme. Several NADH analogs, altered either in the pyridine or purine moiety, functioned as coenzymes. Coenzyme-competitive inhibition by adenosine derivatives demonstrated important interactions of the pyrophosphate region of the coenzyme in binding with the enzyme. Several structural analogs of NADH and pyruvate were evaluated as selective inhibitors of the enzyme. Chemical modification of the purified D-lactate dehydrogenase was effectively achieved by micromolar concentrations of several N-alkylmaleimides. Positive chain length effects in the inactivation by maleimides indicated the presence of a hydrophobic region close to the sulfhydryl groups being modified. The product of the reaction catalyzed by D-lactate dehydrogenase, D(-)-lactate, provides the substrate for a membrane-bound D-lactate oxidase. The D-lactate oxidase converts D(-)-lactate back to pyruvate and transfers electrons to the respiratory chain. No cytosolic L(+)-lactate dehydrogenase was found in Haemophilus influenzae; however, the organism possesses an L-lactate oxidase associated with the cell membrane. The L-lactate oxidase is also part of the respiratory chain, and utilizes exogenous L(+)-lactate to give pyruvate for the organism to use as a carbon source. Haemophilus influenzae and related species have a unique requirement for externally-provided NAD; therefore, several pyridine nucleotide-requiring enzymes become important for the survival of these pathogens. Haemophilus influenzae ATP:NMN adenylyltransferase was partially purified 15-fold with a 27% yield using dye affinity chromatography. Affinity chromatography was also used to purify NAD kinase from Haemophilus influenzae, 18-fold with a 32% yield. Substrate specificity studies of these enzymes demonstrated the enzymes to function with 3-acetylpyridine analogs of their respective substrates. A membrane-bound NMN glycohydrolase was demonstrated in Haemophilus influenzae. The enzyme functions with 3-acetylpyridine mononucleotide as a substrate, and is inhibited effectively by 3-aminopyridine mononucleotide. The possible involvement of this enzyme in the transport of NMN into the cytoplasm is discussed. Growth inhibition studies demonstrated that 3-aminopyridine mononucleotide is a potent inhibitor of growth of the organism and could inhibit growth by inhibiting the transport of NMN. The previously reported inhibition of growth by the 3-aminopyridine adenine dinucleotide was attributed to the formation of the mononucleotide through the reaction catalyzed by the Haemophilus influenzae periplasmic nucleotide pyrophosphatase. A cytosolic lactate dehydrogenase, specific for D(-)-lactate was purified to electrophoretic homogeneity 2100-fold with a 14% yield. The purified enzyme was demonstrated to be a tetramer of M, = 135,000. It catalyzes essentially the reduction of pyruvate with very low activity observed for the oxidation of D(-)-lactate. An optimum pH of 7.2 was determined for the reduction of pyruvate with NADH as the coenzyme. Several NADH analogs, altered either in the pyridine or purine moiety, functioned as coenzymes. Coenzyme-competitive inhibition by adenosine derivatives demonstrated important interactions of the pyrophosphate region of the coenzyme in binding with the enzyme. Several structural analogs of NADH and pyruvate were evaluated as selective inhibitors of the enzyme. Chemical modification of the purified D-lactate dehydrogenase was effectively achieved by micromolar concentrations of several N-alkylmaleimides. Positive chain length effects in the inactivation by maleimides indicated the presence of a hydrophobic region close to the sulfhydryl groups being modified. The product of the reaction catalyzed by D-lactate dehydrogenase, D(-)-lactate, provides the substrate for a membrane-bound D-lactate oxidase. The D-lactate oxidase converts D(-)-lactate back to pyruvate and transfers electrons to the respiratory chain. No cytosolic L(+)-lactate dehydrogenase was found in Haemophilus influenzae; however, the organism possesses an L-lactate oxidase associated with the cell membrane. The L-lactate oxidase is also part of the respiratory chain, and utilizes exogenous L(+)-lactate to give pyruvate for the organism to use as a carbon source.
Ph. D.

9

Clarke, David Morgan. "Pyridine nucleotide transhydrogenase of Escherichia coli: nucleotide sequence of the pnt gene and characterization of the enzyme complex." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27044.

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Based on the rationale that Escherichia coli cells harboring plasmids containing the pnt gene would contain elevated levels of enzyme, three clones were isolated bearing the transhydrogenase gene from the Clarke and Carbon colony bank. The three plasmids were subjected to restriction endonuclease analysis. A 10.4-kilobase restriction fragment which overlapped all three plasmids was cloned into pUC13. Examination of several deletion derivatives of the resulting plasmids and subsequent treatment with exonuclease BAL31 revealed that enhanced transhydrogenase expression was localized within a 3.05-kilobase segment. This segment was located at 35.4 min in the E. coli genome. Plasmid pDC21 conferred on its host 70-fold overproduction of transhydrogenase. The protein products of plasmids carrying the pnt gene were examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of membranes from cells containing the plasmids and by in vitro transcription/translation of pDC21. Two polypeptides of molecular weights 52,000 and 48,000 were coded by the 3.05-kilobase fragment of pDC21. Both polypeptides were required for expression of transhydrogenase activity. The transhydrogenase was purified from cytoplasmic membranes of E. coli by pre-extraction of the membranes with sodium cholate and Triton X-100, solubilization of the enzyme with sodium deoxycholate in the presence of 1 M potassium chloride, and centrifugation through a 1.1 M sucrose solution. The purified enzyme consists of two subunits, α and β, of molecular weights 52,000 and 48,000. During transhydrogenation between NADPH and 3-acetylpyridine adenine dinucleotide by both the purified enzyme reconstituted into liposomes and the membrane-bound enzyme, a pH gradient is established across the membrane as indicated by the quenching of fluorescence of 9-aminoacridine. It was concluded that E. coli transhydrogenase acts as a proton pump which is regulated primarily by a pH gradient rather than a membrane potential. Treatment of transhydrogenase with N,N'-dicyclohexylcarbodiimide results in an inhibition of proton pump activity and transhydrogenation, suggesting that proton translocation and catalytic activities are obligatorily linked. [¹⁴C]Dicyclohexylcarbodiimide preferentially labelled the a subunit. The transhydrogenase-catalyzed reduction of 3-acetylpyridine adenine dinucleotide by NADPH was stimulated over three-fold by NADH. It was concluded that NADH binds to an allosteric binding site on the enzyme. The nucleotide sequences of the pntA and pntB genes, coding for the transhydrogenase αand β subunits respectively, were established. The molecular masses of 53,906 (α) and 48,667 (β) and the N-terminal sequences of the predicted polypeptides agree well with the data obtained by analysis of the purified subunits. Several hydrophobic regions large enough to span the cytoplasmic membrane were observed for each subunit.
Medicine, Faculty of
Biochemistry and Molecular Biology, Department of
Graduate

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Breidenbach, Carl R. "Phospholipid Dependency of Membrane-Associated Pyridine Nucleotide-Utilizing and Succinate Dehydrogenase Activities of Adult Hymenolepis Diminuta (Cestoda) and Ascaris Suum (Nematoda)." Bowling Green State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1343921911.

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Books on the topic "Pyridine nucleotides":

1

David, Dolphin, Avramović Olga, and Poulson Rozanne, eds. Pyridine nucleotide coenzymes: Chemical, biochemical, and medical aspects. New York: Wiley, 1987.

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Jacobson, Kenneth A., and Joel Linden. Pharmacology of purine and pyrimidine receptors. San Diego, CA: Elsevier, 2011.

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Everse, Johannes. Pyridine Nucleotide Coenzymes. Elsevier Science & Technology Books, 2012.

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Sund, Horst. Pyridine Nucleotide-Dependent Dehydrogenases: Proceedings of an Advanced Study Institute Held at the University of Konstanz, Germany, September 15-20 1969. Springer, 2012.

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Dolphin, David, Olga Avramovic, and Rozanne Poulson. Pyridine Nucleotide Coenzymes: Chemical, Biochemical, and Medical Aspects, Part A (Coenzymes and Cofactors, Vol 2). John Wiley & Sons, 1987.

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Pyridine nucleotide coenzymes. New York: Wiley, 1986.

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Pyridine nucleotide coenzymes: Chemical, biochemical and medical aspects. New York: Wiley, 1987.

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Jacobson, Kenneth A., and Joel Linden. Pharmacology of Purine and Pyrimidine Receptors. Elsevier Science & Technology Books, 2011.

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Nucleotide sequence of the pntA and pntB genes encoding the pyridine nucleotide transhydrogenase of 'Escherichia coli'. Berlin: Springer-Verlag, 1986.

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M, Clarke David, ed. Nucleotide sequence of the pnt A and pnt B genes encoding the pyridine nucleotide transhydrogenase of Escherichia coli. New York: Springer-Verlag, 1986.

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Book chapters on the topic "Pyridine nucleotides":

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Passonneau, Janet V., and Oliver H. Lowry. "Pyridine Nucleotides." In Enzymatic Analysis, 3–21. Totowa, NJ: Humana Press, 1993. http://dx.doi.org/10.1007/978-1-60327-407-4_1.

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Petucci, Chris, Jeffrey A. Culver, Nidhi Kapoor, E. Hampton Sessions, Daniela Divlianska, and Stephen J. Gardell. "Measurement of Pyridine Nucleotides in Biological Samples Using LC-MS/MS." In Methods in Molecular Biology, 61–73. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9488-5_7.

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Rustin, Pierre, Michel Neuburger, Roland Douce, and Claude Lance. "The Redox State of Mitochondrial Pyridine Nucleotides Versus Rate of Substrate Oxidation." In Plant Mitochondria, 89–92. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3517-5_12.

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DiPette, D., R. Townsend, J. Guntipalli, K. Simpson, A. Rogers, and E. Bourke. "Effect of Calcium Antagonists on Vasopressin Induced Changes in Myocardial and Renal Pyridine Nucleotides in the Intact Rat." In Myocardial and Skeletal Muscle Bioenergetics, 503–17. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5107-8_38.

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Harding, E. A., C. Kane, R. F. L. James, N. J. M. London, and M. J. Dunne. "Modulation of Three Types of Potassium Selective Channels by NAD and Other Pyridine Nucleotides in Human Pancreatic β-Cells." In Advances in Experimental Medicine and Biology, 43–50. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1819-2_6.

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Lilley, R. McC, A. Goyal, T. Marengo, and A. D. Brown. "The Response of Dunaliella to Salt Stress: A Comparison of Effects on Photosynthesis, and on the Intracellular Levels of the Osmoregulatory Solute Glycerol, the Adenine Nucleotides and the Pyridine Nucleotides." In Progress in Photosynthesis Research, 193–96. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-017-0519-6_42.

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Shibata, K., T. Hayakawa, H. Taguchi, and K. Iwai. "Regulation of Pyridine Nucleotide Coenzyme Metabolism." In Advances in Experimental Medicine and Biology, 207–18. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_19.

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Switzer, Robert L., Howard Zalkin, and Hans Henrik Saxild. "Purine, Pyrimidine, and Pyridine Nucleotide Metabolism." In Bacillus subtilis and Its Closest Relatives, 255–69. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817992.ch19.

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Theorell, H. "Fluorimetric Studies on Pyridine-Nucleotide Enzyme Complexes." In Ciba Foundation Symposium - Significant Trends in Medical Research, 18–42. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719176.ch3.

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Micheli, Vanna, Carlo Ricci, Sylvia Sestini, Marina Rocchigiani, Monica Pescaglini, and Giuseppe Pompucci. "Pyridine Nucleotide Metabolism: Purine and Pyrimidine Interconnections." In Advances in Experimental Medicine and Biology, 323–28. New York, NY: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-7703-4_72.

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Conference papers on the topic "Pyridine nucleotides":

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Masters, Barry R. "Optical Biopsy of Ocular Tissue with Two-Photon Excitation Laser Scanning Microscopy." In Biomedical Optical Spectroscopy and Diagnostics. Washington, D.C.: Optica Publishing Group, 2006. http://dx.doi.org/10.1364/bosd.1996.ft7.

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Abstract:

Two-photon excitation laser scanning microscopy is used to produce three-dimensional maps of cellular metabolism based on the fluorescence of the naturally occurring reduced pyridine nucleotides NAD(P)H. The fluorescence from NAD(P)H was imaged with submicron lateral resolution through the 400 micron thickness of the cornea. Metabolic imaging with two-photon excitation scanning laser microscopy with near-infrared excitation has several advantages over conventional ultraviolet light. The near infrared light can penetrate deeper into the ocular tissue, there is reduced photodamage, and the chromatic aberration that occurred with ultraviolet excitation light is eliminated. In order to confirm that the fluorescence intensity is predominately from the NAD(P)H, the tissues were incubated with cyanide. A subsequent time dependent doubling of the intensity of fluorescence resulted. All cell types in the cornea of an ex vivo eye were imaged. The fluorescence from keratocytes in the corneal stroma was only observed after cyanide treatment. NAD(P)H fluorescence from lens epithelial cells was observed as well as from the lens fibers. These studies demonstrate the validity of using two-photon excitation laser scanning microscopy to perform a noninvasive optical biopsy of ocular tissue.