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Dissertations / Theses on the topic 'Beta-oxidation'

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Published: 4 June 2021
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1

Pourfarzam, Morteza. "#beta#-oxidation of dicarboxylates." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287139.

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2

Ogilvie, Isla Marion. "Enzymes of mitochondrial #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384937.

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3

Ferdinandusse, Sacha. "New insights in peroxisomal [beta]-oxidation." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/64403.

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4

Eaton, Simon. "Regulation of fatty acid #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311443.

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5

Kadlčík, Vojtěch. "Oxidation of beta-amyloid and model peptides." Paris 11, 2006. http://www.theses.fr/2006PA112008.

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Le but de mon travail de thèse était de caractériser les produits de l'oxydation du peptide beta-amyloïde (Abeta) impliqué dans le développement de la maladie d'Alzheimer. Pour étudier l'effet de la structure de peptide sur les processus redox, les propriétés du peptide Abeta (1-40) ont été comparées au peptide de séquence inverse, Abeta (40-1). Les radicaux libres choisis ont été produits en radiolyse gamma. Les produits finaux ont été caractérisés par des techniques d'analyse diverses (HPLC, GC, MALDI-TOF MS, spectrométrie de fluorescence, spectrométrie raman). Pour établir l'effet de l'environnement sur le processus d'oxydation, peptides ont été oxydés dans trois systèmes différents: solution aqueuse homogène, milieu micellaire (SDS) et système des vésicules phospholipidiques (POPC). En solution aqueuse homogène, les produits d'oxydation sont différents pour les deux peptides. Les résidus facilement oxydables sont Met35 pour Abeta(1-40) et Tyr10 pour Abeta(40-1). La présence des micelles ainsi que des vésicules phospholipidiques change profondément le cours de l'oxydation. Une étude structurale en dichroïsme circulaire nous permet d'avancer des hypothèses pour interpréter ces résultats. Nous avons montré que des produits de dégradation des peptides Abeta peuvent induire d'une manière catalytique l'altération des phospholipides. Cette propriété est attribuée à l'action des atomes d'hydrogène sur le peptide. Nos résultats sont intéressants dans le contexte du développement de la maladie d'Alzheimer, car ils peuvent aider à éclairer le rôle de l'interaction de peptide Abeta(1-40) avec des membranes phospholipidique dans les propriétés redox du peptide
The goal of my thesis work was to characterize oxidation products of beta-amyloid peptide (Abeta), which is implied in the development of Alzheimer's disease. To study the effect of peptide structure on the redox processes, oxidation properties of Abeta(1-40) were compared to the peptide with reverse sequence, Abeta(40-1). Azide and hydroxyl radicals used for oxidation were produced by gamma radiolysis. Final products were characterized by a variety of analytical techniques (HPLC, GC, MALDI-TOF MS, fluorescence and raman spectrometry). To establish the role of peptide environment on its redox properties, oxidation was carried out in three different systems: homogeneous aqueous solution, micellar system (SDS) and in the presence of phospholipids vesicles (POPC). In homogeneous aqueous solution, oxidation products are different for both peptides. The main oxidation targets are Met35 for Abeta(1-40) and Tyr10 for Abeta(40-1). The presence of micelles and phospholipid vesicles has an important impact on the oxidation pathways. These changes could be related to changes in peptide conformations studied by circular dichroism. We have also shown that Abeta degradation products may catalytically induce alternation of phospholipids. This process is initiated by reaction of hydrogen radicals with the peptide. Our results are interesting in the context of the development of Alzheimer's disease as they may bring an insight into the role of Abeta(1-40) interaction with phospholipids membrane for the redox properties of the peptide
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6

Lee, Wai Ming. "Oxidation reactions and antioxidant properties of #Beta#-carotene." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237679.

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7

Creswick, Heather Alison. "The Oxidation of beta-Cyclodextrin Via the Photolysis of 6-beta-Cyclodextrin Benzoyl Formate." W&M ScholarWorks, 1993. https://scholarworks.wm.edu/etd/1539625808.

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8

Watmough, N. J. "Measurement of intermediates and products of fatty acid #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234411.

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9

Heath, Christine Evelyn. "The Selective Oxidation of beta-Cyclodextrin on the Secondary Face." W&M ScholarWorks, 1997. https://scholarworks.wm.edu/etd/1539626108.

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10

Grunsven, Elisabeth Gerarda van. "Functions and dysfunctions of peroxisomal fatty acid [beta]-oxidation in man." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/82102.

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11

Weil, Kerstin. "3-(R)-Hydroxysäuren als Produkte selektiven Fettsäureabbaus Studien zur [beta]-Oxidation in Stenotrophomonas maltophilia /." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=964105012.

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12

Roermund, Carolus Wilhelmus Thomas van. "Fatty acid [beta]-oxidation in Saccharomyces cerevisiae new insights with implications for human diseases /." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/62779.

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13

Cheignon, Clémence. "Oxidation of the amyloid-beta peptide and consequences on the etiology of Alzheimer's disease." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30347/document.

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La maladie d'Alzheimer (MA) est la forme la plus fréquente de démence chez les personnes âgées. L'une de ses caractéristiques est la formation extracellulaire de plaques séniles dans le cerveau des malades, composées du peptide Amyloïde-ß (Aß) sous forme agrégée et d'ions métalliques tels que le cuivre. Le peptide Aß forme un complexe avec les ions cuivre, capable de catalyser la formation d'espèces réactives de l'oxygène (ERO), en présence d'un réducteur tel que l'ascorbate. Ces espèces oxydantes sont délétères pour les molécules environnantes, ainsi que pour le peptide Aß lui-même. Etant proche du site de production des ERO, Aß est une cible privilégiée, notamment pour le radical hydroxyle HO*. L'objectif de ce travail a été d'étudier la réaction de production des ERO par le système Aß/Cu/ascorbate, de caractériser les dommages oxydatifs subis par Aß et d'évaluer les conséquences de l'oxydation de Aß sur la production des ERO, la coordination des ions métalliques et l'agrégation. Différentes techniques spectroscopiques ont été utilisées, notamment la spectrométrie de masse (MS), la spectroscopie de fluorescence, la résonnance paramagnétique électronique (RPE) et l'absorption de rayons X (XANES). Les sites d'oxydation du peptide Aß ont été étudiés par spectrométrie de masse (MS et MS/MS). Grâce à l'utilisation des outils de la protéomique et de la spectrométrie de masse à haute-résolution (HRMS), les acides aminés oxydés du peptide Aß ont été identifiés. Ainsi, Asp1, His13 et His14 sont les cibles privilégiées de l'attaque de HO*. Ce résultat était attendu puisque ces résidus sont impliqués dans la coordination du cuivre, par l'intermédiaire duquel les ERO sont directement générées. L'impact de l'oxydation du peptide sur la coordination des ions métalliques Cu(II), Cu(I) et Zn(II), la production de ERO ainsi que sur l'agrégation du peptide a été étudié. Les résultats ont montré que l'oxydation du peptide induit un changement de coordination du Zn(II) ainsi que des deux états d'oxydation du cuivre, menant à une augmentation de la production de ERO. De plus, l'oxydation de Aß a également un impact sur l'agrégation, ne privilégiant pas la formation de fibrilles. Le mode de coordination du complexe Cu-Aß lors de la production des ERO a été déduit de l'étude d'une série de peptides Aß comprenant un ou plusieurs acides aminés mutés. L'hypothèse proposant que les acides aminés oxydés sont ceux liés au cuivre lors de la production des ERO (Asp1, His13 et 14) a été renforcée, la mutation de Asp1 ou des deux His13 et 14 ayant un impact direct sur la production des ERO. Enfin, les effets pro- et anti-oxydants de l'ascorbate ont été étudiés, montrant que, sur le système Cu-Aß, l'ascorbate n'exerce ses propriétés anti-oxydantes qu'à forte concentration pour les molécules environnantes, mais qu'il n'a aucun effet protecteur sur le peptide Aß lui-même
Alzheimer's Disease (AD) is the most frequent for of dementia in the elderly. A hallmark of AD is the extracellular formation of senile plaques in the brain of AD subjects, composed of the Amyloid-ß peptide (Aß) under aggregated form with metal ions such as copper ions. Aß can form a complex with copper ions, able to catalyze reactive oxygen species (ROS) formation in the presence of a reducing agent such as ascorbate. These oxidative species can oxidize the surrounding molecules and the Aß peptide itself. Being close to the production site of ROS, Aß is the preferential target, especially for the hydroxyl radical HO*. The aim of this work was to study the ROS production by the Aß/Cu/ascorbate system, to characterize the oxidation undergone by Aß and to evaluate the consequences of Aß oxidation on ROS production, metal ions coordination and aggregation. Several spectroscopic techniques have been used, in particular mass spectrometry (MS), fluorescence spectroscopy, electron paramagnetic resonance (EPR) and X-Ray absorption spectroscopy (XANES). The oxidation sites of Aß have been studied by mass spectrometry (MS and MS/MS). Thanks to the use of proteomic tools and high-resolution mass spectrometry (HRMS), the oxidized amino acid residues have been identified. Asp1, His 13 and His14 have been found to be the preferential targets for HO* on Aß. This result was expected as these residues are involved in copper coordination, from which the ROS are generated. The impact of Aß oxidation on Cu(II), Cu(I) and Zn(II) on metal ions coordination, on ROS production and on Aß aggregation has been studied. Results have shown that Aß oxidation induces a change of coordination of Zn(II) as well as Cu(II) and Cu(I), leading to an increase of ROS production. Moreover, Aß oxidation has also an impact on aggregation, as it does not favor fibrils formation. The Cu-Aß binding mode during ROS production has been deduced from the study of a series of mutated Aß peptides. The hypothesis, in which the amino acid residues bound to Cu during the ROS production are the oxidized one (Asp1, His 13 and His14) has been corroborated by the results of this study, the mutation of Asp1 or the two His having an impact on ROS production. Finally, the pro- and antioxidants effects of ascorbate have been investigated, showing that, on the Cu-Aß system, ascorbate only has antioxidant properties at high concentration for surrounding molecules, but does not exhibit any protecting effect on Aß itself
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14

Kanase, Nilesh. "The impact of oxidative stress and potential antioxidant therapy on function and survival of cultured pancreatic β-islet cells." Thesis, University of the Highlands and Islands, 2011. https://pure.uhi.ac.uk/portal/en/studentthesis/the-impact-of-oxidative-stress-and-potential-antioxidant-therapy-on-function-and-survival-of-cultured-pancreatic-islet-cells(ec0cd703-3902-4410-8c58-e7c7e49f33e7).html.

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Dietary antioxidant curcumin derived from turmeric has been suggested to decrease the risk of many chronic diseases. Much of the existing data for curcumin stem from experiments performed at supra-physiological concentrations (μM-mM) that are impossible to attain through oral ingestion. It was therefore hypothesized that curcumin at low plasma achievable concentration, though itself not acting as a direct antioxidant might up-regulate the intracellular antioxidants and thus helping combat oxidative stress and protect β-islet cells. The results indicated that Curcumin, DMC and BDMC were able to scavenge hydroxyl radicals, but showed little scavenging ability against superoxide and nitric oxide radicals. Nanomolar concentrations of curcuminoids easily prevented the deleterious effects of H2O2 in pancreatic β-islet RINm5F cells. Non of the curcuminoids showed a detrimental effect on insulin secretion, but the model did not allow assessment of any potential positive effect on insulin secretion. The findings confirmed that nanomolar concentrations of curcumin offered protection in pancreatic β-islet cells against H2O2-indicated damage by modulating the proportion of oxidised GSH (GSSG): reduced GSH in the favour of GSH and the increasing the activity of SOD. This increase in GSH and SOD levels was, at least in part, on account of an increase in GR, SOD-1 and SOD-2 gene expression. The intracellular mechanism driving this modulation of antioxidant gene was, by virtue of blocking the H2O2  induced NF-κB activation.
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15

Epshteyn, Albert. "Synthesis, stability, and reactivity of high-oxidation-state pentamethylcyclopentadienyl acetamidinate [beta]-Hydride- or [beta]-Methide-bearing alkyl complexes of zirconium, titanium, and tantalum." College Park, Md. : University of Maryland, 2006. http://hdl.handle.net/1903/4249.

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Thesis (Ph. D.)--University of Maryland, College Park, 2006.
Thesis research directed by: Chemistry. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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16

Pallikarana, Tirumala Harini. "Role of mitochondrial beta-oxidation in ethanol response: A candidate gene study using Caenorhabditis elegans." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4993.

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Alcohol use disorder (AUD) is the fourth leading cause of preventable death in the United States, and the fifth leading risk factor for premature death and disability, globally. There are currently very few treatment options for AUD and there is a need for effective preventive and treatment strategies for this condition. AUD risk has a significant hereditary component, with the contribution of genetic factors being estimated to be about 50%. The Davies-Bettinger laboratory uses C. elegans as a model organism to study the contribution of genetic factors in modulating neuronal responses to ethanol. In this project, we examined the role of mitochondrial beta-oxidation of fatty acids (FA) in altering ethanol responses using loss-of-function (lf) mutants and RNAi-mediated knockdown of specific genes in this pathway. We tested a total of 34 genes and found that lf in 13 genes significantly affected ethanol response phenotypes. We conclude that mitochondrial beta-oxidation of FA is essential for ethanol response behavior in C. elegans. Further experiments need to be conducted to dissect the specific contribution of various components of mitochondrial beta-oxidation in modifying the neuronal responses to ethanol.
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17

Mathieu, Magali. "Structure determination of thiolase." Châtenay-Malabry, Ecole centrale de Paris, 1995. http://www.theses.fr/1995ECAP0424.

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La structure de la 3-kétoacyl-CoA thiolase péroxisomale de la levure S. Cerivisiae a été tout d'abord déterminée à une résolution de 2. 8A. Il y a un dimère par unité asymétrique, et il fut essentiel pour la détermination de cette structure de mettre à profit l'axe de rotation d'ordre 2 reliant les deux monomères de thiolase. Chaque monomère de thiolase (417 résidus) est composé de trois domaines. Les domaines N- et C- terminaux ont la même topologie: un feuillet béta formé de cinq brins-béta et recouvert d'hélices. Le troisième domaine (domaine-l) forme une longue boucle en surface et entoure le site actif. Ce domaine est incomplet à 2. 8a. Des expériences réalisées à 100k permirent de collecter un jeu de données complet à 1. 8a. Le raffinement de la structure de thiolase à cette résolution n'est pas terminée, mais la structure intermédiaire obtenue possède un monomère contenant un domaine-L complet, permettant de proposer un modèle de l'interaction du ligand acyl-CoA avec le site actif de la thiose.
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18

Qin, Y. M. (Yong-Mei). "Molecular characterization of peroxisomal multifunctional 2-enoyl-CoA hydratase 2/(3R)-hydroxyacyl-CoA dehydrogenase (MFE type 2) from mammals and yeast." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:951425337X.

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Abstract Fatty acid degradation in living organisms occurs mainly via the β-oxidation pathway. When this work was started, it was known that the hydration and dehydrogenation reactions in mammalian peroxisomal β-oxidation were catalyzed by only multifunctional enzyme type 1 (MFE-1; Δ2-Δ3-enoyl-CoA isomerase/2-enoyl-CoA hydratase 1/(3S)-hydroxyacyl-CoA dehydrogenase) via the S-specific pathway, whereas in the yeast peroxisomes via the R-specific pathway by multifunctional enzyme type 2 (MFE-2; 2-enoyl-CoA hydratase 2/(3R)-hydroxyacyl-CoA dehydrogenase). The work started with the molecular cloning of the rat 2-enoy-CoA hydratase 2 (hydratase 2). The isolated cDNA (2205 bp) encodes a polypeptide with a predicted molecular mass of 79.3 kDa, which contains a potential peroxisomal targeting signal (AKL) in the carboxyl terminus. The hydratase 2 is an integral part of the cloned polypeptide, which is assigned to be a novel mammalian peroxisomal MFE-2. The physiological role of the mammalian hydratase 2 was investigated with the recombinant hydratase 2 domain derived from rat MFE-2. The protein hydrates a physiological intermediate (24E)-3α, 7α, 12α-trihydroxy-5β-cholest-24-enoyl-CoA to (24R, 25R)-3α, 7α, 12α, 24-tetrahydroxy-5β-cholestanoyl-CoA in bile acid synthesis. The sequence alignment of human MFE-2 with MFE-2(s) of different species reveals 12 conserved protic amino acid residues, which are potential candidates for catalysis of the hydratase 2. Each of these residues was replaced by alanine. Complementation of Saccharomyces cerevisiae fox-2 (devoid of endogenous MFE-2) with human MFE-2 provided a model system for examing the in vivo function of the variants. Two protic residues, Glu366 and Asp510, of the hydratase 2 domain of human MFE-2 have been identified and are proposed to act as a base and an acid in catalysis. Mammalian MFE-2 has a (3R)-hydroxyacyl-CoA dehydrogenase domain, whereas the yeast MFE-2 has two dehydrogenase domains, A and B. The present work, applying site-directed mutagenesis to dissect the two domains, shows that the growth rates of fox-2 cells expressing a single functional domain are lower than those of cells expressing S. cerevisiae MFE-2. Kinetic experiments with the purified proteins demonstrate that domain A is more active than domain B in catalysis of medium- and long-chain (3R)-hydroxyacyl-CoA, whereas domain B is solely responsible for metabolism of short-chain substrates. Both domains are required when yeast cells utilize fatty acids as the carbon source.
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19

Sidibe, Amadou. "Analyses protéomiques d'une communauté bactérienne du sol et de Rhodanobacter thiooxydans se développant en présence de subérine de pomme de terre." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/8060.

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Résumé: La subérine, un polymère lipidique et complexe des plantes est retrouvé dans divers tissus dont le périderme de la pomme de terre. Le processus biologique de sa dégradation reste encore peu connu et est attribué aux champignons. Des échantillons de sol provenant d'un champ de pommes de terre ont été inoculés dans un milieu de culture contenant de la subérine comme source de carbone. Une approche métaprotéomique a été utilisée pour identifier les populations bactériennes qui se développent en présence de la subérine sur une période d'incubation de 60 jours. Le nombre de spectres normalisé (NSpC) des protéines extracellulaires produites par la communauté bactérienne du sol ont considérablement diminué du jour 5 au jour 20, puis ont augmenté lentement, révélant une succession de bactéries, où la population des bactéries du genre Pseudomonas à croissance rapide a diminué et a été remplacée par d’autres espèces bactériennes qui pouvaient se développer en présence de la subérine. La récalcitrance de la subérine a été démontrée par l'émergence de bactéries auxotrophes telles qu’Oscillatoria dans les derniers jours de la culture bactérienne. Néanmoins, l'identification de deux lipases dans le surnageant de la culture suggère qu'au moins certaines espèces bactériennes peuvent dégrader la subérine. Une des lipases (I4WGM2) a été associée à Rhodanobacter thiooxydans. Lorsque cultivée dans un milieu contenant de la subérine, la souche de R. thiooxidans LCS2 a produit trois lipases, dont I4WGM2. R. thiooxidans LCS2 a également produit d'autres protéines liées au métabolisme des lipides, des transporteurs de chaines d’acide gras et les enzymes de la [béta]-oxydation. Ceci suggère que R. thiooxydans pourrait participer à la dégradation de la subérine.
Abstract: Suberin is a complex lipidic plant polymer found in various tissues including potato periderm. The biological degradation process of suberin is poorly characterized and is attributed to fungi. Soil samples from a potato field were used to inoculate a culture medium containing suberin as carbon source and a metaproteomics approach was used to identify bacterial populations that develop in the presence of suberin, over a 60-day incubation period. The normalized spectral counts of predicted extracellular proteins produced by the soil bacterial community drastically decreased from day 5 to day 20 and then slowly increased, revealing a succession of bacteria. The population of fast-growing pseudomonads declined and was replaced by species that could develop in the presence of suberin. The recalcitrance of suberin was demonstrated by the emergence of auxotrophic bacteria such as Oscillatoria in the last days of the assay. Nevertheless, the identification of two putative lipases in the culture supernatants suggests that at least some bacterial species could degrade suberin. One of the lipases (I4WGM2) was associated with Rhodanobacter thiooxydans. When grown in a suberin-containing medium, R. thiooxydans strain LCS2 produced three lipases, including I4WGM2. This strain also produced other proteins linked to lipid metabolism, including fatty acid and lipid transporters and [beta]-oxidation enzymes, suggesting that R. thiooxydans could participate in suberin degradation.
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20

Yong, Chee Heng. "Inhibition of beta-oxidation of fatty acids in rat ventricular trabeculae and the effects of the action potential." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295509.

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21

Bursby, Timothy Patrick. "Investigations of the mitochondrial #beta#-oxidation trifunctional protein and its association with complex 1 of the respiratory chain." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364807.

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22

Stockunas, Michelle Marie. "The Effects of Interval Training and Modest Calorie Restriction in the Treatment of Obesity." Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/35011.

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Moderate intensity exercise (MIT) was compared to high intensity interval exercise (HIIT) as part of a nine week treatment strategy for 13 obese men. Both groups exercised three days per week beginning at 45% VO2max. The MIT protocol progressed to 65% VO2max by week eight. The HIIT protocol consisting of 16 short (30 s), 8 medium (90 s), and 4 long (180 s) intervals progressed to 110% VO2max, 100% VO2max, and 90% VO2max, respectively, by week nine with low intensity intervals at 40% VO2max. Exercise duration of the MIT group was adjusted to allow for energy expenditure equal to that of the HIIT group. Modest dietary restriction and weekly group nutrition education sessions were part of the treatment. Weight decreased similarly by 2.4% in the MIT group and 2.8% in the HIIT group (p<0.05). For the groups combined, exercise resulted in a 7% decrease in body fat percent (%BF) and a 9% decrease in fat mass (FM) (p<0.05). There was no difference in the change in %BF or FM for either group. There were no changes in fat free mass (FFM) over the treatment or between groups. Waist circumference decreased 2.8% overall with no differences between the two groups (p<0.05). There were no differences in waist-to-hip ratio (WHR) or waist-to-thigh ratio (WTR) due to the intervention. The activity of vastus lateralis b 3-hydroxyacyl CoA dehydrogenase (HADH) increased 37% and 97% (p<0.05) for the MIT and HIIT groups respectively with a trend for differences between the two groups (p=0.055). The results show that an exercise program of moderate or high intensity is effective to cause weight reduction. The data suggest that HIIT may be more effective over a longer treatment period if the observed trend for greater capacity for muscle fat oxidation translates into improved body fat loss.
Master of Science
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23

Roberts, Lee D. "Defining the metabolic effect of peroxisome proliferator-activated receptor δ activation." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/226743.

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Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors that function as ligand activated transcription factors. There are three identified isotypes: PPAR alpha, PPAR gamma and PPAR delta, together controlling the expression of genes involved in inflammation, cell differentiation, proliferation, lipid and carbohydrate metabolism and energy homeostasis. The PPARs are potential targets for the treatment of dyslipidaemia, type II diabetes mellitus and the metabolic syndrome. This thesis uses a multi-platform metabolomics approach, 13C-isotope substrate flux analysis, respirometry and transcriptomics to determine the role PPAR delta and PPAR gamma play in metabolic control both in adipose tissue and systemically. To achieve this, the metabolic phenotype of the 3T3-L1 adipocyte cell line was defined to generate a metabolically phenotyped in vitro model of adipose tissue. The importance of fatty acid alpha-oxidation in the differentiation of adipocytes was emphasised The effects of PPAR delta and PPAR gamma activation in white adipose tissue from the ob/ob mouse model of insulin resistance, and in the phenotyped 3T3-L1 adipocyte model, were investigated. PPAR delta activation was distinguished by oxidative catabolism of fatty acids and citric acid cycle intermediates. Conversely, PPAR gamma activation was identified by the sequestration of lipids into adipose tissue. Moreover, to address the systemic influence of PPAR activation, with a focus on the Cori cycle and the interactions of the liver and skeletal muscle, the metabolic changes that occur in these tissues following PPAR delta and PPAR gamma activation in the ob/ob mouse were examined. PPAR delta activation was characterised by the mobilisation and release of triacylglycerols (TAGs) into circulation as an energy source for peripheral tissues whereas PPAR gamma activation was defined by a reduction and sequestration of circulating TAGs. This thesis has better characterised the role of the PPARs as master regulators of metabolism and emphasised their potential as therapeutic targets for metabolic diseases of global importance.
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24

Osiki, Prisca Ofure. "The effect of beta-oxidation or TCA cycle inhibition on mitochondrial function and the sensitivity of high resolution respiratory detection." Master's thesis, Faculty of Health Sciences, 2019. http://hdl.handle.net/11427/30944.

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INTRODUCTION: A dysfunction in fatty acid beta-oxidation (β-oxidation), particularly medium chain acyl-CoA dehydrogenase (MCAD) dysfunction is a major cause of mortality and its diagnosis is usually achieved by measuring specific protein activities or metabolites in blood and/or urine samples. However, these methods do not account for secondary defects that accompany primary deficiency; such as where measures of disruption in fatty acid metabolism do not account for defects in the TCA cycle and oxidative phosphorylation. These metabolic pathways are connected and dysfunction in one pathway (primary) could lead to dysfunction in the other (secondary). We propose the use of methods that combines all aspects of the bioenergetics module (enzyme activity in substrate oxidation within each individual pathway, transfer of electrons through the electron transport system (ETS) and oxidative phosphorylation for ATP generation) may be a more effective assessment technique. High resolution respirometry (HRR) is a recently developed technique that accounts for substrate oxidation, electron transfer via the ETS and oxidative phosphorylation. It measures the rate of oxygen consumption or flux at different respiratory states when appropriate substrates, uncouplers and inhibitors (SUIT protocols) are used. With this method, two substrate combinations are commonly used to assess medium-chain fatty acid β-oxidation; a) Octanoylcarnitine and carnitine, which is partial to the β-oxidation cycle alone, and b) Octanoylcarnitine and malate, which assesses the influence of the TCA cycle. Additionally, a combination of pyruvate, glutamate and malate is used to assess oxidation within the TCA cycle. We investigated the sensitivity of commonly used substrate combinations in HRR assessment to detect changes in mitochondrial respiration and dysfunction induced by the inhibition of either β-oxidation or the TCA cycle in C2C12 myotubes. Furthermore, we assessed MCAD, citrate synthase and aconitase enzyme activities when β-oxidation or TCA cycle was inhibited in C2C12 myotubes. METHODS: C2C12 myotubes were differentiated for 6 days and treated for 12 hours with a high or a low concentration of one of two inhibitors as follows; a) 2 mM or 8 mM 2-mercaptoacetate to inhibit medium chain acyl-CoA dehydrogenase (MCAD); b) 6 mM or 9 mM fluorocitrate to inhibit aconitase. Each treatment was compared to control myotubes grown for the same length of time without the addition of inhibitors. The activities of MCAD, aconitase and citrate synthase were determined. In addition, mitochondrial respiration measured as O2 flux at Routine, Leak, OXPHOS and ETS respiratory states were assessed in an Oxygraph-2K after inhibition or in control treatments using; i) Octanoylcarnitine and carnitine ii) Octanoylcarnitine and malate iii) pyruvate, malate and glutamate substrate combinations. For each assessment we corrected O2 flux recorded at each state to; a) approximate number of cells (pmol O2/s/million cells) b) protein concentration (pmol O2/s/mg protein) c) Flux control ratio (FCR) of each state to the maximum ETS capacity; ETSFAO+CI+CII (convergent electron flow from Fatty acid oxidation (FAO), Complex I (CI) and CII) d) FCR to either FAO-linked ETS capacity; (ETSFAO) or CI-linked ETS capacity (ETSCI). RESULTS: Treatment of cells with either a low or high concentration of 2-mercaptoacetate to inhibit MCAD resulted in no significant difference in MCAD activity. Fluorocitrate treatment decreased aconitase activity with low treatment (p = 0.011) compared to control, and conversely it increased MCAD activity in high treatment compared to control (p = 0.024). Both 2-mercaptoacetate (p = 0.03) and fluorocitrate (p < 0.01) treatment at high concentrations resulted in increased citrate synthase activity, compared to low concentration and control. Mitochondrial respiration with octanoylcarnitine and carnitine substrate combination was not altered with MCAD or aconitase inhibition. Octanoylcarnitine and malate substrate combination showed a decrease in mitochondrial respiration at the following respiratory states with both MCAD and aconitase inhibition; Routine (p = 0.01), LeakFAO (p = 0.029), OXPHOSFAO (p = 0.006), ETSFAO (p = 0.008), ETSFAO+CI (p = 0.017). FCR of each state to the maximum capacity (ETSFAO+CI+CII) revealed a decrease with both MCAD and aconitase inhibition at the following states; routine (p = 0.001), OXPHOSFAO (p = 0.003), ETSFAO (p = 0.018), ETSFAO+CAR (p = 0.008) and ETSFAO+CI (p = 0.027). Pyruvate, malate and glutamate substrate combination showed decreased mitochondrial respiration with MCAD inhibition at the following respiratory states; Routine (p = 0.004), LeakCI (p = 0.007), OXPHOSCI (p = 0.003), ETSCI (p = 0.003), ETSCI+FAO (p = 0.01) and ETSCI+FAO+CII (p = 0.003). FCR of each state to the maximum capacity (ETSCI+FAO+CII) decreased with both MCAD and aconitase inhibition at Routine (p = 0.024), OXPHOSCI (p = 0.024) and ETSCI (p = 0.035) states. DISCUSSION: The main finding of this study was related to two of the SUIT protocols 1) octanoylcarnitine and malate, and 2) pyruvate, malate and glutamate. These protocols were sensitive in showing decreased respiratory capacity and coupling control ratios and may be appropriate for assessing changes in oxidative metabolism when there is a defect in β-oxidation and/ or the TCA cycle. On the other hand, octanoylcarnitine and carnitine substrate combination is not sensitive to detect dysfunction induced by inhibition of either β-oxidation or TCA cycle. Irrespective of the enzyme inhibited, HRR detected dysfunction in complex I (CI), although, when aconitase was inhibited, reduced CI-linked respiration was more pronounced compared to MCAD inhibition. Furthermore, primary inhibition of MCAD to inhibit β-oxidation may have caused secondary inhibition of TCA cycle via aconitase, shown in decreased TCA cycle CI-linked respiration where MCAD was inhibited. In contrast, primary inhibition of aconitase seemed to be compensated for by increased MCAD activity and mitochondrial respiration related to β-oxidation. Lastly, enzyme assaysshould not be used as standalone techniques for assessing metabolic dysfunction at the level of TCA, β-oxidation and the mitochondria since they are not sensitive to low level defects, nor do they account for secondary interactions that influence either TCA or betaoxidation. HRR is useful to assess mitochondrial respiration and dysfunction, when using an appropriate substrate combination and should be used in combination with the more traditional enzyme activity assays.
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25

Pfluger, Paul Thomas. "Der Metabolismus der Tocopherole und Tocotrienole." Phd thesis, kostenfrei, 2007. http://opus.kobv.de/ubp/volltexte/2008/1601/.

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26

Jenkins, Benjamin John. "The role of alpha oxidation in lipid metabolism." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278025.

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Recent findings have shown an inverse association between the circulating levels of pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0) with the risk of pathological development in type 2 diabetes, cardio vascular disease and neurological disorders. From previously published research, it has been said that both these odd chain fatty acids are biomarkers of their dietary intake and are significantly correlated to dietary ruminant fat intake. However, there are profound studies that show the contrary where they do not display this biomarker correlation. Additionally, several astute studies have suggested or shown odd chain fatty acid endogenous biosynthesis, most often suggested via alpha oxidation; the cleavage of a single carbon unit from a fatty acid chain within the peroxisomes. To better understand the correlations and interactions between these two fatty acids with pathological development, the origin of these odd chain fatty acids needed to be determined, along with confirming their association with the disease aetiology. To minimise animal & human experimentation we made use of existing sample sets made available through institutional collaborations, which produced both animal and human interventional study samples suitable for odd chain fatty acid investigations. These sample collaborations allowed us to comprehensively investigate all plausible contributory sources of these odd chain fatty acids; including from the intestinal microbiota, from dietary contributions, and derived from novel endogenous biosynthesis. The investigations included two intestinal germ-free studies, two ruminant fat diet studies, two dietary fat studies and an ethanol intake study. Endogenous biosynthesis was assessed through: a stearic acid infusion, phytol supplementation, and an Hacl1 knockout mouse model. A human dietary intervention study was used to translate the results. Finally, a study comparing circulating baseline C15:0 and C17:0 levels with the development of glucose intolerance. We found that the circulating C15:0 and C17:0 levels were not significantly influenced by the presence or absence of intestinal microbiota. The circulating C15:0 levels were significantly and linearly increased when the C15:0 dietary composition increased; however, there was no significant correlation in the circulating C17:0 levels with intake. Circulating levels of C15:0 were affected by the dietary composition and factors affecting the dietary intake, e.g. total fat intake and ethanol, whereas circulating C17:0 levels were found to be independent of these variables. In our studies, the circulating C15:0 levels were not significantly affected by any expected variations in alpha oxidation caused by pathway substrate inhibition or gene knockout. However, C17:0 was significantly related, demonstrating it is substantially endogenously biosynthesised. Furthermore, we found that the circulating C15:0 levels, when independent of any dietary variations, did not correlate with the progression of glucose intolerance when induced, but the circulating C17:0 levels did significantly relate and linearly correlated with the development of glucose intolerance. To summarise, the circulating C15:0 and C17:0 levels were independently derived; the C15:0 levels substantially correlated with its dietary intake, whilst the C17:0 levels proved to be separately derived from its endogenous biosynthesis via alpha oxidation of stearic acid. C15:0 was found to be minimally endogenously biosynthesised via a single cycle of beta oxidation of C17:0 in the peroxisomes, however, this did not significantly contribute to the circulating levels of C15:0. Additionally, only the baseline levels of C17:0 significantly correlated with the development of glucose intolerance. These findings highlight the considerable differences between both of these odd chain fatty acids that were once thought to be homogeneous and similarly derived. On the contrary, they display profound dietary, metabolic, and pathological differences.
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27

Garrett, Hannah Mary. "A study into the influence of amyloid-beta peptide oxidation on the rate of fibril formation, with a synthesis of 2-oxo-histidine." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8485.

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The Amyloid Cascade Hypothesis states that fibrillation of the amyloid beta (Aβ) peptide is the primary cause of Alzheimer’s pathology. The trigger for the fibrillation is a subject of much debate, although it is clear, oxidative stress is a key feature of Alzheimer’s aetiology. This thesis explores a possible role of oxidation of Aβ, in particular the effect of histidine and methionine side-chain oxidation, on Aβ fibril growth rates. Within chapters 2 and 3 of this thesis is a discussion of various approaches to chemical synthesis of 2-oxo-histidine with a view to the incorporation of the oxidised amino acids into Aβ peptide using Fmoc approaches. Chapter 2 describes attempted chemical transformation of (protected) L-histidine into L-oxohistidine. Dimethyldioxirane oxidised Boc-His-OMe yielded products containing isopropylidene groups, while oxidation using a Cu(II)/ascorbate generated 2-oxo-histidine but gave very low yields. Within chapter 3, a successful synthesis of protected 2-oxo-histidine is described, via the known imidazolin-2-one-4-carboxylic. Chapter 4 analyses Aβ(1-40) fibrillation kinetics by treating the intact peptide with various oxidants. Contrary to previous reports, hydrogen peroxide alone did not slow fibrillation rates. Cu(II)/Cu(I)- catalysed oxidation increased the likelihood of amorphous aggregation over fibrillation. This thesis shows oxidation of Aβ has a profound influence on fibril growth and that incorporation of a stable oxidised histidine into Aβ is a realisable goal.
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28

Portolesi, Roxanne, and roxanne portolesi@flinders edu au. "Fatty acid metabolism in HepG2 cells: Limitations in the accumulation of docosahexaenoic acid in cell membranes." Flinders University. Medicine, 2007. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20070802.103146.

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The current dietary recommendations for optimal health are designed to increase our intake of two bioactive omega-3 (n-3) fatty acids, eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3), abundant naturally in fatty fish such as salmon. Health authorities recommend that the general population consume two to three fatty fish meals per week (1) for optimal health and for the prevention of cardiovascular disease. However, some modern Western societies consume only modest amounts of fish and seafood (2;3). Land based vegetable oils may provide an alternative to meet these needs. Linseed and canola oils are rich in alpha-linolenic acid (ALA, 18:3n-3) (4). ALA can be converted endogenously to EPA and DHA and suggests that increasing the dietary intake of ALA may increase the conversion and accumulation of DHA in tissues and plasma. However, elevated dietary intakes of ALA in animals and humans results in an increased level of EPA in tissues yet there is little or no change in the level of DHA (5-7). The current consensus is that the synthesis of DHA from ALA in humans is limited yet the mechanisms involved in regulating the accumulation of DHA in tissues are poorly understood. The reputed rate-limiting enzyme in the conversion of fatty acids is delta 6 desaturase (D6D). ALA is a substrate for D6D and undergoes a series of desaturation and elongation reactions to yield n-3 long chain polyunsaturated fatty acids (LCPUFA). The final step in the synthesis of DHA from ALA involves translocation of its immediate fatty acid precursor, 24:6n-3 from the endoplasmic reticulum to the peroxisome to be partially beta-oxidised to yield DHA. The involvement of multiple enzymes in the desaturation-elongation pathway, and the integration of other pathways, such as phospholipid biosynthesis, suggests there are various steps that may regulate the accumulation of DHA in cell membranes. This thesis aimed to examine the possible regulatory steps in the conversion of fatty acids to LCPUFA, particularly in the synthesis of DHA from n-3 fatty acid precursors. The human hepatoma cell line, HepG2, was used as an in vitro cell system to examine the accumulation of individual fatty acids and their metabolites in isolation from other competing fatty acid substrates. The accumulation of linoleic acid (LA, 18:2n-6) and ALA in HepG2 cell phospholipids following supplementation with increasing concentrations of each respective fatty acid correlated with that described in vivo, as was the accumulation of their conversion products. The accumulation of DHA in cells supplemented with ALA reached a plateau at concentrations above 5 micro g/ml and paralleled the accumulation of 24:6n-3 in cell phospholipids, suggesting that the delta 6 desaturation of 24:6n-3 was prevented by increasing concentrations of ALA, thereby limiting the accumulation of DHA. The accumulation of DHA in cells supplemented with eicosapentaenoic acid (EPA, 20:5n-3) or docosapentaenoic acid (DPA, 22:5n-3) was significantly greater than the level of DHA that accumulated in cells supplemented with ALA. However, regardless of substrate, the level of DHA in cell membranes reached a plateau at substrate concentrations above 5 micro g/ml. This thesis further aimed to examine the effect of fatty acid supplementation on the mRNA expression of D6D in HepG2 cells. The expression and activity of D6D mRNA is subject to nutritional and hormonal regulation. The mRNA expression of D6D in HepG2 cells following supplementation with oleic acid (OA, 18:1n-9), LA, ALA, arachidonic acid (AA, 20:4n-6) or EPA was examined by real time RT PCR. The expression of D6D mRNA was reduced by up to 50% in cells supplemented with OA, LA, ALA , AA or EPA compared with control cells and suggests that fatty acids modulate the expression of the key enzyme involved in the conversion of fatty acids. The effect of fatty acid co-supplementation on the fatty acid composition of HepG2 cell phospholipids was also examined in an attempt to gain insights into the role of D6D and the enzymes involved in peroxisomal beta-oxidation on the accumulation of DHA from n-3 fatty acid precursors. The reduction in the accumulation of DHA in cells co-supplemented with DPA and docosatetraenoic acid (DTA, 22:4n-6) was greater than in cells co-supplemented with DPA and LA, suggesting that peroxisomal beta-oxidation may have a greater role in determining the accumulation of DHA from DPA than the activity of D6D. Further investigation should be directed towards understanding the role that peroxisomal beta-oxidation may play in the synthesis of DHA from precursor fatty acids. The fatty acid composition of cell membranes in vivo is a result of several physiological processes including dietary intake, phospholipids biosynthesis and fatty acid conversion as well as catabolic processes. This thesis demonstrates that a greater understanding of the regulation of the conversion of fatty acids will help to define dietary approaches that enhance the synthesis of n-3 LCPUFA from n-3 fatty acid precursors to lead to improved outcomes for health.
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29

Sherwood, Roger. "Exploring reactivity of four square planar beta-ketoaminato cobalt compounds in the [+1, +2, +3] oxidation states with applications to controlled radical polymerization and lignin degradation." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44330.

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30

Moreira, Alini Schultz. "Benefício da natação em modelo experimental de doença gordurosa hepática não alcoólica e síndrome metabólica." Universidade do Estado do Rio de Janeiro, 2010. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=3344.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
O acúmulo crônico de gordura no fígado (doença hepática gordurosa não alcoólica ou esteatose hepática não alcoólica - NAFLD) está fortemente associada com a obesidade e a resistência à insulina. O estudo teve como objetivo investigar o efeito do exercício físico (natação) na redução da esteatose hepática e comorbidades associadas, incluindo a expressão hepática de síntese de ácidos graxos e receptor proliferador de peroxissoma atividade alfa. Camundongos machos C57BL/6 foram divididos em dois grandes grupos de acordo com a dieta durante 22 semanas: dieta padrão (10% de gordura, SC) ou dieta rica em gordura (60% de gordura, HF), caracterizando os grupos sedentários SC-Sed e HF-Sed. Nas últimas 10 semanas do experimento, metade dos grupos sedentários foram submetidos ao protocolo de natação com um aumento progressivo no tempo (6/dia até 60/dia, 5x/semana), caracterizando os grupos exercitados: SC-Ex e HF-Ex. No final do experimento, comparado ao grupo SC-Sed, o grupo HF-Sed teve a massa corporal significativamente superior, hiperglicemia, hiperinsulinemia com resistência à insulina, hipertrofia dos adipócitos (com infiltrado inflamatório), hipertrofia das ilhotas pancreáticas, dislipidemia, alteração das enzimas hepáticas e inflamatórias e NAFLD com mudanças na expressão de proteínas hepáticas lipogênicas e oxidativas. O programa de natação, mesmo concomitante com a dieta rica em gordura, reduziu o excesso de peso e todos os outros resultados, especialmente a NAFLD. Os resultados permitem concluir que a natação pode atenuar os efeitos deletérios de uma dieta rica em gorduras combinado com estilo de vida sedentário em camundongos. Estes dados reforçam a idéia que o exercício físico pode ser considerado uma estratégia terapêutica não farmacológica eficaz no tratamento da NAFLD, obesidade e resistência à insulina.
Chronic accumulation of fat in the liver (nonalcoholic fatty liver disease or NAFLD) is a morbid condition strongly associated with obesity and insulin resistance. The study aimed to investigate the effect of swimming training in reducing the NAFLD and associated comorbidities, including the hepatic expression of fatty acid synthesis and peroxisome proliferator receptor activity-alpha . Male C57BL/ 6 mice were separated into two major groups according to their nutrition and studied during 22 weeks: standard chow (10% fat, SC) or high fat chow (60% fat, HF), characterizing the sedentary groups SC-Sed and HF- Sed. In the last 10 weeks of the experiment, half of the sedentary groups were submitted to a swimming training with a progressive increase in duration, characterizing the exercised groups: SC-Ex and HF-Ex. At the end of the experiment, considering the findings in the SC-Sed group, HF-Sed group had significantly higher body mass, hyperglycemia, hyperinsulinemia with insulin resistance, hypertrophy of the adipocytes (with inflammatory infiltrate), hypertrophy of the pancreatic islets, dyslipidemia, altered liver enzymes and inflammatory cytokines, and NAFLD with changes in gene expression of hepatic lipogenic and oxidative proteins. The swimming program, even concomitant with the high-fat diet, reduced overweight and all the other worst findings, especially NAFLD. The results allow the conclusion that swimming training can attenuate the morbid effects of a high-fat diet combined with sedentary lifestyle in mice. These data reinforce the notion that swimming exercise can be considered an efficient nonpharmacologic therapy in the treatment of NAFLD, obesity and insulin resistance.
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31

Guzun-Cojocaru, Tatiana. "Peroxydation des lipides émulsionnés et transfert d'ions fer à l'interface huile / eau stabilisée par des protéines de lait : influence des résidus phosphates et de la stabilité du chélate de fer." Thesis, Dijon, 2010. http://www.theses.fr/2010DIJOS012/document.

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Le fer ajouté dans des systèmes complexes tels que les aliments induit divers problèmes comme l'oxydation des lipides ou la précipitation d’autres composés présents dans la matrice. Il s’en suit une diminution de sa biodisponibilité et des défauts de goût. L'utilisation de chélates de fer, comme le bisglycinate de fer ou l’EDTA de fer, constitue une voie intéressante : le fer ainsi protégé n’interagirait pas avec la matrice alimentaire. La stabilité des chélates de fer (bisglycinate de fer et NaFe EDTA), supposés peu réactif pour l’initiation de peroxydation, a été attestée sur des modèles d’émulsions huile dans eau stabilisées par du caséinate de sodium ou de la β lactoglobuline. Dans un second temps, le travail a consisté à vérifier la faible influence de ces complexes sur la nature de l’interface huile/eau (étude de la tension et de la rhéologie interfaciales). La stabilité du bisglycinate de fer en solution aqueuse et en présence de β lactoglobuline a également été évaluée en fonction du pH (pH 2, 3,5 et 6,5) par rayons X. Il a ainsi été montré que la nature des protéines formant l’interface huile/eau et le type de sels de fer jouent un rôle crucial sur la stabilité oxydative des émulsions enrichies en fer. L'affinité des protéines de lait pour les ions fer libres est le premier facteur qui contrôle la peroxydation des matières grasses par l’absence de transfert à l'interface huile/eau. La capacité du complexe bisglycinate à retenir les ions fer et donc à limiter la présence d’ions fer libres (ferriques ou ferreux) apparaît comme le second facteur principal à contrôler. La compétition pour les ions fer entre les groupes fonctionnels des protéines et les contre ions de chélates (glycinate ou EDTA) gouverne ainsi l'état d'oxydation du système dans des conditions acide/base proche de la neutralité. En milieu acide, l'oxydation est principalement gouvernée par l’instabilité du complexe bisglycinate de fer et par conséquent la lente libération fer ionique dans la phase aqueuse. Pour résumer, si le complexe de fer n’est pas déstabilisé et que la protéine à l’interface huile/eau ne présente pas de groupe fonctionnel ayant une forte affinité pour le fer, alors la peroxydation des lipides en émulsion est faible. Dans notre démonstration, si une protéine n’est pas phosphorylée et pour des pH proches de 7, alors l’émulsion ne sera pas peroxydée car le fer ne migre pas à l’interface huile/eau
Iron incorporated into food systems induces oxidation and precipitation. The consequences are a reduced bioavailability and a modification of other food flavor. The iron chelates such as Fe-bisglycinate and Fe-EDTA represent a possibility to avoid side effects, since the iron is protected. The inertety of Fe bisglycinate and NaFe EDTA for lipid peroxidation has been verified in oil-in-water emulsion models stabilized by sodium caseinate or by β lactoglobulin through the following studies: i/ increase of primary and secondary products of oxidation, ii/ change of the properties of the oil/water interface (tension and interfacial rheology), iii/ the stability of the chelate iron (Fe-bisglycinate) in the aqueous phase with β lactoglobulin at different pH (pH 2, 3.5 and 6.5). The oil/water interface stabilized by proteins with phosphate groups has induced peroxidation, which was not observed with proteins containing no phosphate residue. These results demonstrate also that the type of iron salts plays a crucial role in the oxidative stability of emulsions. The ability of the complex to retain iron ion and to avoid “free” ferrous ion is the first important factor to be controlled. The affinity of milk proteins to bind these free iron ions is the second factor that controls the transfer to oil/water interface. To sum up, the competition for iron ions between functional groups of protein and salt counter ions (glycinate, sulfate or EDTA) governs the oxidation state of the system in neutral conditions. In acidic medium, the oxidation is mainly governed by the stability of the complex and the possibility to free iron in bulk
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Farhat, Elie. "Physiological Responses of Goldfish and Naked Mole-Rats to Chronic Hypoxia: Membrane, Mitochondrial and Molecular Mechanisms for Metabolic Suppression." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42595.

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Chronic hypoxia is a state of oxygen limitation that is common in many aquatic and terrestrial environments. Metabolic suppression is an essential strategy that is used by hypoxia-tolerant champions such as goldfish and naked mole-rats to cope with prolonged low oxygen. This thesis examines the physiological processes used by goldfish and naked mole-rats to survive in low oxygen environments. It proposes a novel mechanism - the remodeling of membrane lipids - to reduce ATP use and production. Temperature (homeoviscous adaptation), diet (natural doping in migrant birds) and body mass (membrane pacemaker of metabolism) have an impact on the lipid composition of membranes that, in turn, modulates metabolism. In chapters 2 and 3 of this thesis, I demonstrate that vertebrate champions of hypoxia tolerance undergo extensive changes in membrane lipid composition upon in vivo exposure to low oxygen. These changes and those observed in hibernating mammals can promote the downregulation of Na⁺/K⁺-ATPase (major ATP consumers), mitochondrial respiration capacity [OXPHOS (phosphorylating conditions), proton leak (non-phosphorylating conditions), cytochrome c oxidase], and energy metabolism (β-oxidation and glycolysis) as discussed in chapters 3 and 4. A common membrane signal regulating the joint inhibition of ion pumps and channels could be an exquisite way to preserve the balance between ATP supply and demand in hypometabolic states. In chapter 5, I show that the reduction in ATP turnover is also orchestrated by mechanisms that involve post-translational and post-transcriptional modifications and epigenetic changes. Membrane remodeling, together with these more traditional molecular mechanisms, could work in concert to cause metabolic suppression.
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33

Alaimo, Joseph. "Identification and Characterization of Ethanol Responsive Genes in Acute Ethanol Behaviors in Caenorhabditis elegans." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/549.

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Alcohol abuse and dependence are complex disorders that are influenced by many genetic and environmental factors. Acute behavioral responses to ethanol have predictive value for determining an individual’s long-term susceptibility to alcohol abuse and dependence. These behavioral responses are strongly influenced by genetics. Here, we have explored the role of genetic influences on acute behavioral responses to ethanol using the nematode worm, Caenorhabditis elegans. First, we explored the role of ethanol metabolism in acute behavior responses to ethanol. Natural variation in human ethanol metabolism machinery is one of the most reported and reproducible associations found to alter drinking behavior. Ethanol metabolism is conserved across phyla and alteration in this pathway alters acute behavioral responses to ethanol in humans, mice, rats, and flies. We have extended these findings to the worm and have shown that loss of either alcohol dehydrogenase or aldehyde dehydrogenase results in an increase in sensitivity to the acute effects of ethanol. Second, we explored the influence of differences in basal and ethanol-induced gene expression in ethanol responsive behaviors. We identified a set of candidate genes using the basal gene expression differences in npr-1(ky13) mutant animals to enrich for genes involved in AFT. This analysis revealed ethanol changes to the expression of genes involved in a variety of biological processes including lipid metabolism. We focused on a gene involved in the metabolism of fatty acids, acs-2. acs-2 encodes an acyl-CoA synthetase that activates fatty acids for mitochondrial beta-oxidation. Animals carrying mutant acs-2 have significantly reduced AFT and we explored the role of genes in the mitochondria beta-oxidation pathway for alterations in ethanol responsive behaviors. We have shown that knockdown of ech-6, an enoyl-CoA hydratase, enhances the development of AFT. This work has uncovered a role for fatty acid utilization pathways in acute ethanol responses and we suggest that natural variation in these pathways in humans may impact the acute alcohol responses to alcohol that in turn influence susceptibility to alcohol abuse and dependence.
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34

Zezina, Lilija. "Mechanisms and treatment options of chronic graft dysfunction : Experimental and clinical studies." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4959-X/.

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35

Zondervan, Charon. "Homogeneous catalytic oxidation a ligand approach /." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 1997. http://irs.ub.rug.nl/ppn/298195445.

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36

Habarou, Florence. "Métabolisme de l'acétyl-CoA : modulation pharmacologique, approches thérapeutiques et nouvelles maladies." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB104.

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L’acétyl-coA occupe une place centrale dans le métabolisme intermédiaire. Il constitue le point de jonction de plusieurs voies métaboliques telles que la .-oxydation, la glycolyse, le catabolisme de certains acides aminés, la cétolyse, la cétogenèse et la synthèse d’acides gras. Il est également impliqué dans d’autres processus tels que l’acétylation des protéines. Au cours de mon travail de thèse, je me suis attachée à étudier différents aspects du métabolisme de l’acétyl-coA. La première partie de mon travail a porté sur la modulation pharmacologique de la .- oxydation dans le but de corriger des déficits de cette voie métabolique. L’intérêt de traitements par 400µM de bézafibrate ou 75µM de resvératrol dans les formes modérées de déficit en VLCAD et en CPT2 avait été montré précédemment. Par des méthodes de référence et grâce à la mise au point de nouvelles techniques, j’ai pu montrer sur des fibroblastes de patients déficitaires en LCHAD que des traitements par une combinaison de 35µM de bézafibrate et 30µM de resvératrol permettent d’augmenter les capacités d’oxydation du palmitate en stimulant la synthèse protéique. L’effet de cette combinaison était comparable à celui d’un traitement par 400µM de bézafibrate. Dans un second temps, je me suis intéressée à deux cofacteurs impliqués dans le métabolisme de l’acétyl-coA : l’acide lipoïque, cofacteur de quatre .-cétoacides déshydrogénases (PDHc, BCKDHc, .- KGDHc et GCS) et la riboflavine, cofacteur d’acyl-coA déshydrogénases de la .-oxydation et de déshydrogénases impliquées dans le catabolisme des acides aminés ramifiés. Ainsi, j’ai participé à la description d’anomalies du métabolisme de l’acide lipoïque, un nouveau groupe de maladies héréditaires du métabolisme caractérisé par un déficit combiné en .-cétoacides déshydrogénases. Par ailleurs, j’ai pu montrer qu’une hyperprolinémie constitue un biomarqueur intéressant pour le diagnostic d’acidurie glutarique de type II primaire ou secondaire, ces dernières pouvant se rencontrer en cas d’anomalie du métabolisme de la riboflavine. J’ai également évalué l’utilisation d’un mélange racémique de L,D-3-hydroxybutyrate afin de corriger les déficits énergétiques induits par un déficit en PDHc ou GLUT1. Via la cétolyse, le L,D-3- hydroxybutyrate génère de l’acétyl-coA. De façon surprenante, l’administration de ce composé s’est traduite par une amélioration de l’état clinique des patients atteints de déficits en PDHc, alors qu’une dégradation a été observée chez les patients atteints de déficits en GLUT1. Cette évolution différente pourrait souligner l’importance de l’anaplérose chez les patients déficitaires en GLUT1. Enfin, la dernière partie de mon travail de thèse porte sur la description d’un patient atteint d’une forme modérée de déficit en pyruvate carboxylase, cette enzyme étant régulée par l’acétyl-coA. Les difficultés diagnostiques rencontrées devant ces formes modérées sont rapportées, ainsi que des essais de traitement par des composés anaplérotiques et par le bézafibrate, malheureusement sans bénéfice net que ce soit in vitro ou in vivo. En conclusion, le métabolisme de l’acétyl-coA est altéré dans de nombreuses maladies héréditaires du métabolisme, dont certaines sont de description récente. Il peut être modulé par différentes approches pharmacologiques. Le développement de nouvelles techniques et notamment les analyses de flux métaboliques fournissent des outils utiles à son exploration et à l’étude de nouveaux traitements
Acetyl-CoA is crucial for intermediary metabolism. It is at the crossroad of several metabolic pathways such as beta-oxidation, glycolysis, aminoacid catabolism, ketolysis, and fatty acid synthesis. It is also involved in other processes such as protein acetylation. In this document I studied different aspects of acetyl-CoA metabolism. First, I tried to correct fatty acid oxidation defects through pharmacological approach. Thanks to well- known methods and new ones, I showed that a combination of 30µM resveratrol and 35µM bezafibrate increased fatty acid oxidation capacities by increasing protein synthesis, as well as 400µM bezafibrate. Acetyl-CoA metabolism is also altered due to cofactors defects such as lipoic acid or riboflavine deficiency. I was involved in new diseases description and research for new biomarkers in this context. PDHc and GLUT1 deficiency are two different diseases with the same consequence : a defect in acetyl- CoA production from glucose. In order to improve patients’ quality of life, I evaluated the substitution of ketogenic diet with a racemic mix of L,D-3-hydroxybutyrate in PDHc and GLUT1 deficiency. The clinical evolution of patients was strikingly different, with an improvement in PDHc patients, whereas a degradation was noticed in GLUT1 patients. This difference might underline the role of anaplerosis in GLUT1 deficiency. Finally, I evaluated anaplerotic treatment and bezafibrate treatment in pyruvate carboxylase deficiency, an enzyme allosterically regulated by acetyl-CoA. To conclude, acetyl-CoA metabolism is altered in numerous inherited errors of metabolism, some of them being recently described. It can be modulated by pharmacological approaches. The development of new techniques such as metabolic flux analysis are useful for its study and for new treatments evaluation
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37

Golozar, Mehdi. "Plasma electrolytic oxide coatings on low-modulus [beta]-type titanium alloys : applications to load-bearing orthopaedic implants." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709079.

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38

Burton, Robert M. "Oxidant concentration effects in the hydroxylation of phenol over titanium-based zeolites Al-free Ti-Beta and TS-1." Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/2366.

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Thesis (MScEng (Process Engineering))--University of Stellenbosch, 2006.
This work focuses on the effects of hydrogen peroxide concentration on the catalytic activity and product selectivity in the liquid-phase hydroxylation of phenol over titanium-substituted zeolites Al-free Ti-Beta and TS-1 in water and methanol solvents. Hydroquinone is typically the desired product, and these solvents employed have previously been shown to be of importance in controlling the selectivity of this reaction. Different volumetric quantities of an aqueous 30 wt-% peroxide solution were added to either water or methanol solutions containing the catalyst and phenol substrate, and the reaction monitored by withdrawing samples over a period of 6-8 hours. For Al-free Ti-Beta catalysed reactions, the peroxide concentration affects the selectivity and activity differently in water and methanol solvents. Using methanol solvent, the selectivity to hydroquinone formation is dominant for all peroxide concentrations (p/o-ratio > 1), and favoured by higher initial peroxide concentrations (> 1.27 vol-%), where p/o-ratios of up to can be reached; in water solvent, increasing the peroxide concentration above this level results in almost unchanging selectivity (p/o-ratio of ca. 0.35). For lower peroxide concentrations in water, the p/o-ratio increases slightly, but never exceeds the statistical distribution of ca. 0.5. Using water as a solvent, higher phenol conversion is obtained as the initial peroxide concentration increases; in methanol the phenol conversion is largely independent of peroxide concentration. As expected for the smaller pore TS-1, higher hydroquinone selectivity is obtained in methanol than for Al-free Ti-Beta, which is consistent with shape-selectivity effects enhanced by the use of this protic solvent. Interestingly, with TS-1 the p/o-ratio is higher at lower phenol conversions, and specifically when the initial peroxide concentration is low (p/o-ratio exceeding 3 were obtained at low phenol conversion), and decreases to a near constant value at higher conversions regardless of the starting peroxide concentration. Thus, low peroxide concentrations favour hydroquinone formation when TS-1 is used as the catalyst. Comparing the performance of the two catalysts using methanol solvent, the phenol conversion on TS-1 is more significantly influenced by higher hydrogen peroxide concentrations than Al-free Ti-Beta. However, with higher initial concentrations the unselective phenol conversion to tars is more severe since the hydroquinone selectivity is not higher at these high peroxide concentrations. The increased tar formation, expressed as tar deposition on the catalyst or as the tar formation rate constant, confirms that the greater amount of free-peroxide present is mainly responsible for the non-selective conversion of phenol. Kinetic modelling of the reaction data with an overall second-order kinetic model gave a good fit in both solvents, and the phenol rate constant is independent of changing hydrogen peroxide concentration for the hydroxylation over Al-free Ti-Beta using water as the solvent (kPhenol = 1.93 x 10-9 dm3/mmol.m2.s). This constant value suggests that the model developed to represent the experimental data is accurate. For TS-1 in methanol solvent the rate constant is also independent of peroxide concentration (kPhenol = 1.36 x 10-8 dm3/mmol.m2.s). The effect of the method of peroxide addition was also investigated by adding discrete amounts over a period of 4.5 hours, and was seen to improve hydroquinone selectivity for reaction on both catalysts, and most significantly for Al-free Ti-Beta in methanol solvent. With TS-1, the mode of peroxide addition had little influence on phenol conversion, but the initial selectivity to hydroquinone was ca. 1.6 times higher than for an equivalent single-portion addition (at a similar phenol conversion). Discrete peroxide addition for hydroxylation in methanol over Al-free Ti-Beta gave greatly improved hydroquinone selectivities compared to the equivalent single-dose addition. Compared to TS-1, the initial selectivity was not as high (p/o-ratios of 0.86 and 1.40 respectively at 10 mol-% phenol conversion), but this can be explained on the basis of geometric limitations in the micropores of TS-1 favouring hydroquinone formation. The final selectivity, however, is marginally higher (using the same mode of peroxide addition, and at the same phenol conversion). Discrete peroxide addition has an additional benefit in that it also reduces the quantity of free-peroxide available for product over-oxidation, and consequently reduces the amount of tars formed. Thus, the interaction of the effects of peroxide concentration and the solvent composition and polarity on the product selectivity and degree of tar formation is important. Particularly with TS-1, lower peroxide concentrations in bulk methanol solvent are highly beneficial for hydroquinone formation, because of the implicit geometric constraints in the micropores, the lower water concentration, and the decreased tar formation associated with high methanol concentrations. This could have significant reactor design implications, as the results obtained here suggest that the reaction should be terminated after approximately 30 minutes to maximise hydroquinone production (under the conditions evaluated in these experiments), even though the corresponding phenol conversions are low (ca. 10 mol-%). The higher hydroquinone selectivities reached at low phenol conversions for the discrete peroxide addition experiments also confirm this. Practically, to enhance the hydroquinone selectivity for reaction over TS-1, the initial phenol-peroxide molar ratio should be ca. 10, methanol should constitute not less than 90 vol-% of the reaction volume, and the peroxide should be added in discrete amounts. For reaction over Al-free Ti-Beta, methanol solvent also enhances the hydroquinone formation as expected. At low phenol conversions (ca. 10 mol-%) hydroquinone is still the preferred product, although in contrast to TS-1 the selectivity increases with phenol conversion, and is higher with higher initial peroxide concentrations. Under the best conditions evaluated here for optimal hydroquinone formation, the initial phenol-peroxide molar ratio should be ca. 2.5, with methanol making up at least 90 vol-% of the total volume. Discrete peroxide addition in methanol solvent for the Al-free Ti-Beta catalysed hydroxylation gives excellent improvements in hydroquinone selectivity (2.5 times higher than water solvent), and the addition in more discrete portions might further improve hydroquinone formation, and should therefore be examined.
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39

Kahef, Lana el. "Oxydation des mesotetraphenyl porphyrines : beta-substitution par voie electrochimique directe." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13221.

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40

Pereira, Renata de Oliveira. "Formação de subprodutos do estrona e 17\'beta\'-estradiol na oxidação utilizando cloro e o ozônio em água." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/18/18138/tde-07042011-134759/.

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A poluição dos corpos de água é cada vez maior devido ao lançamento de efluentes, esgotamento sanitário e disposição inadequada de resíduos sólidos. Esse fato causa grande preocupação à comunidade científica, pois à poluição associam-se riscos à saúde causado por poluentes bioativos, compostos químicos orgânicos persistentes e outros compostos que poderiam estar presentes na água. Dentre as substâncias que causam risco à saúde se destacam os desreguladores endócrinos, que são compostos químicos exógenos que interferem na atividade hormonal. Os sistemas de tratamento de água convencionais não removem alguns compostos, tais como pesticidas e hormônios, os quais deveriam ser removidos. O uso do ozônio e cloro vem sendo reportado para tal finalidade, pois atuam como oxidantes que são capazes de oxidar compostos orgânicos, além de serem poderosos desinfetantes. Portanto, o objetivo deste estudo foi avaliar a eliminação e/ou redução dos desreguladores endócrinos - DE em estações de tratamento de água com o uso do ozônio e do cloro. Aliado ao estudo, avaliar qual será a eficiência de remoção de organismos indicadores nas doses utilizadas para oxidação de DE (Coliformes Totais e E.coli) e avaliar a ecotoxicidade em peixes de amostras cloradas contendo 17\'beta\'-estradiol. O cloro e o ozônio foram capazes de remover eficientemente estrona (E1) e 17\'beta\'-estradiol (E2) de águas, contudo a eficiência de remoção diminui em concentrações na ordem de ng/L, necessitando-se de altas doses de ozônio e cloro para a completa remoção dos hormônios estudados. Tanto o cloro como o ozônio foram eficientes na inativação de organismos indicadores nas doses comumente utilizadas em ETAs e nas doses requeridas para a remoção dos contaminantes estudados. Amostras contendo E2 após serem cloradas apresentaram toxicidade crônica a peixes da espécie Danio rerio, o efeito estrogênico foi observado principalmente em machos. Foi necessário uma dose de ozônio de 0,95 e 3,8 mg/L para a remoção de 93 e 98% de E2 e E1 respectivamente (Co = 100 ng/L). Considerando o cloro como oxidante após a aplicação de 1,5 mg/L com tempo de contato de 24 h chegou-se a uma remoção de 99,6 e 97,5% para o E2 e E1 respectivamente (Co = 500 ng/L). Tão importante quanto remover o estrona e o 17\'beta\'-estradiol foi verificar e identificar quais foram os subprodutos formados após a oxidação dos mesmos. Foram identificados vários subprodutos tanto utilizando a degradação por meio do cloro como do ozônio. Alguns destes compostos identificados foram persistentes e recalcitrantes. Para o ozônio a completa remoção foi atingida após 10 mg/L de \'O IND.3\' e 16 mg/L de \'O IND.3\' para os subprodutos do E1 e E2 respectivamente. Considerando o cloro mesmo após um tempo de contato de 16 dias, havia ainda subprodutos da degradação na água.
The pollution of water bodies is increasing due to the release of effluents, sewage and inadequate solid waste disposal. This fact causes great concern to the scientific community, because pollution are associated with health risks caused by pollutants of bioactive compounds and other persistent organic compounds that could be present in water. Among the substances that can cause health risks are the endocrine disrupters, which are exogenous chemicals that interfere with hormonal activity. The conventional water treatment systems does not remove certain compounds, such as pesticides and hormones, which should be removed. The use of ozone and chlorine has been reported for this purpose because it acts as an oxidant that can oxidize organic compounds, and addicionally are powerful disinfectants. Therefore, the aim of this study was the elimination and/or reduction of endocrine disrupters during the water treatment using ozone and chlorine. Allied to the study, evaluate the efficiency of indicator organisms removal in the doses used for the oxidation of endocrine disrupters (coliform and E.coli) and assess the ecotoxicity of fish in chlorinated samples containing 17\'beta\'- estradiol. Chlorine and ozone were able to efficiently remove estrone (E1) and 17\'beta\'-estradiol (E2) of water, but the removal efficiency decreases at concentrations in the ng/L. Complete removal of the hormones was reach with high doses of ozone and chlorine. Both chlorine and ozone were effective in the inactivation of indicator organisms at commonly doses used in water treatment plants and in the doses required for the removal of the pollutants studied. Samples containing chlorinated E2 had chronic toxicity to fish Danio rerio, the estrogenic effect was observed mainly in males, females in some groups estrogenic effect was not observed. The dose of ozone necessary for the removal of 93 and 98% of E1 and E2 (Co = 100 ng/L) were 0.95 and 3.8 mg/L, respectively. The application of 1.5 mg/L of chlorine with a contact time of 24 h achieved removal of 99.6 and 97.5% for E1 and E2 respectively (Co = 500 ng/L) . As important as removing estrone and 17\'beta\'-estradiol was to verify and identify which were the byproducts formed after oxidation. Several byproducts were identified by the degradation using chlorine and ozone. Some of these compounds were identified to be persistent and recalcitrant. The ozone dose required to the complete removal of the byproducts was achieved after 10 mg/L \'O IND.3\' and 16 mg/L \'O IND.3\' for the byproducts of E1 and E2 respectively. The byproducts of chlorine even after a contact time of 16 days persisted in the water.
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41

Gurak, Poliana Deyse. "Degradação térmica e química de beta-caroteno e sua relação com a capacidade antioxidante e propriedades de cor." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/256395.

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Orientador: Adriana Zerlotti Mercadante
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia de Alimento
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Resumo: Muitos processos utilizados na indústria de alimentos empregam altas temperaturas e proporcionam o contato dos alimentos com substâncias pró-oxidantes. Tais condições tornam a sequência de ligações duplas conjugadas presente nos carotenoides susceptível à isomerização geométrica, oxidação e degradação. Portanto, o objetivo principal deste trabalho foi estudar a degradação térmica e química do b-caroteno, através da identificação dos compostos primários de degradação e sua relação com a capacidade antioxidante e as propriedades de cor. Os experimentos realizados foram: a) aquecimento a 120 °C na presença de ar; b) aquecimento a 120 °C sob fluxo de oxigênio, c) aquecimento a 120 °C na presença de ar e adição de galato de propila; d) aquecimento a 150 °C na presença de ar; e) aquecimento a 150 °C sob fluxo de oxigênio; f) aquecimento a 150 °C sob fluxo de nitrogênio; g) clivagem oxidativa com permanganato de potássio (KMnO4) e h) reação de epoxidação com ácido meta-cloro-perbenzóico (MCPBA). A degradação do b-caroteno foi monitorada através da análise de carotenóides totais por espectrofotometria, a avaliação da cor por colorimetria (parâmetros CIELAB) e análise do perfil de carotenóides por cromatografia líquida de alta eficiência com detectores de arranjo de fotodiodos e espectrometria de massas (HPLC-DAD-MS/MS). As alterações na capacidade antioxidante foram avaliadas por meio da capacidade de desativação do radical ABTS¿+ (2,2¿-azinobis-(3-etilbenzotiazolina-6-sulfonato)) e da proteção contra o oxigênio singlete (1O2) utilizando o 9,10-dimetil-antraceno como actinômetro e azul de metileno como sensibilizador. Foram identificados 16 carotenóides gerados pela degradação térmica e química do b-caroteno. O aquecimento resultou na diminuição da concentração de all-trans-b-caroteno com a formação de isômeros (13-cis, 9-cis, 15-cis, 9,13-di-cis, 9,15-di-cis, 9,13¿-di-cis, 13,15-di-cis-ß-caroteno), epóxidos (5,6 e 5,8-epóxi-ß-caroteno) e, em menor quantidade, apocarotenóides (ß-apo-8¿-carotenal, ß-apo-10¿-carotenal, ß-apo-12¿-carotenal). Na oxidação química com KMnO4, o all-trans-b-caroteno foi totalmente degradado após 30 min de reação com formação de b-apo-8¿-carotenal, b-apo-10¿-carotenal, b-apo-12¿-carotenal, b-apo-15-carotenal e semi-b-carotenona. Já na reação com MCPBA, o all-trans-b-caroteno não foi completamente degradado e os produtos de degradação formados em maior proporção foram 5,6-epóxi-b-caroteno, 5,6:5¿,6¿-diepóxi-b-caroteno, 5,6:5¿,8¿-diepóxi-b-caroteno e 5,8-epóxi-b-caroteno, além de pequena quantidade de 13-cis-b-caroteno e 9-cis-b-caroteno. Em todos os experimentos foi observada a existência de correlação superiores a 0,91 entre alguns parâmetros físicos de cor (b* e C*ab) e o parâmetro químico (teor de carotenóides totais), indicando que estes parâmetros de cor podem ser utilizados para monitorar a degradação de carotenóides. O mecanismo proposto para os dois tipos de degradação (térmica e química) envolveu reações reversíveis e irreversíveis, para formação de compostos de isomerização e de oxidação, respectivamente. A análise da capacidade antioxidante mostrou que a presença isolada de b-caroteno ou a mistura de b-caroteno com produtos de degradação térmica apresentaram valores similares de TEAC (capacidade antioxidante equivalente a trolox) e de porcentagem de proteção contra 1O2. Por outro lado, os produtos de oxidação gerados na reação química com KMnO4 resultaram em um aumento nos valores de TEAC e maior eficiência da desativação do 1O2 com o aumento do tempo de reação
Abstract: Many processes in the food industry aplly high temperatures and allow the contact with pro-oxidant substances, such conditions in which the sequence of conjugated double bonds, present in carotenoids, is susceptible to geometric isomerization, oxidation and degradation. Therefore, the main aim of this work was to study the thermal and chemical degradation of b-carotene, identifying the primary degradation compounds and its relation with the antioxidant capacity and colour properties. The experiments were: a) heating at 120 °C with air exposure; b) heating at 120 °C under flow of pure oxygen; c) heating at 120 °C with air exposure and addition of propyl gallate; d) heating at 150 °C with air exposure; e) heating at 150 °C under flow of pure oxygen; f) heating at 150 °C under a flow of pure nitrogen; g) oxidative cleavage with potassium permanganate (KMnO4); and h) epoxidation with meta-chloroperbenzoic acid (MCPBA). In all experiments, the degradation and formation of isomerization and oxidation products were monitored by analysis of total carotenoids by spectrophotometer, colour evaluation by colorimetry and carotenoid profile analysis by high-performance liquid chromatography with photodiode array detector and mass spectrometry (HPLC-DAD-MS). Changes in the antioxidant capacity were monitored by the scavenging capacity against the ABTS¿+ (2,2-azinobis(3-ethylbenzthiazoline-6-sulphonic acid)), and protection against singlet oxygen (1O2) using 9,10-dimethyl-anthracene as actinometer and methylene blue as sensitizer. A total of sixteen carotenoids were identified in both the chemical and thermal degradation of b-carotene. Heating caused a decrease in the all-trans-b-carotene content with the formation of cis isomers (13-cis, 9-cis, 15-cis, 9,13-di-cis, 9,15-di-cis, 9,13¿-di-cis, 13,15-di-cis-b-carotene), epoxides (5,6 and 5,8-epoxy-b-carotene) and apocarotenoids (b-apo-8'-carotenal, b-apo-10'-carotenal, b-apo-12'-carotenal). The chemical degradation with KMnO4 completely degraded the all-trans-b-carotene in 30 minutes of reaction, with the formation of b-apo-8'-carotenal, b-apo-10'-carotenal, b-apo-12'-carotenal, b-apo-15-carotenal and semi-b-carotenone. In the reaction with MCPBA, all-trans-b-carotene was not completely degraded and the major products were 5,6-epoxy-b-carotene, 5,6:5¿,6¿-diepoxy-b-carotene, 5,6:5¿,8¿-diepoxy-b-carotene and 5,8-epoxy-b-carotene, with small amounts of 13-cis-b-carotene and 9-cis-b-carotene. All experiments showed correlations above 0.91 between some physical colour parameters (b* and C*ab) and chemical parameters (content of total carotenoids), indicating that some colour parameters can be used to monitor carotenoid degradation. The proposed mechanism in both types of degradation (thermal and chemical) involved reversible and irreversible reactions, to the formation of isomerization and oxidation compounds, respectively. The analysis of the antioxidant capacity showed that both pure b-carotene and the mixture of b-carotene with thermal degradation products had similar values of TEAC (trolox equivalent antioxidant capacity), as well as similar protection percentage against 1O2. On the other hand, the products formed in the chemical reaction with KMnO4 resulted in increase in both the TEAC values and protection against 1O2 with the increase in reaction time
Doutorado
Ciência de Alimentos
Doutor em Ciência de Alimentos
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42

Chen, Ming-Wei. "Laser Spectroscopy Studying Organic and Inorganic Intermediates in The Atmospheric Oxidation Process." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1316196649.

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43

HOUTTEVILLE, MARIE-CLAIRE. "Etude de la simple et de la double diastereoselectivite de la reaction d'aldolisation de l'acide propanedithioique : synthese de beta-oxodithioesters par oxydation chimioselective de beta-hydroxydithioesters." Caen, 1988. http://www.theses.fr/1988CAEN2006.

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44

Denis, Isabelle. "Photodégradation des composés organiques volatils biogéniques dans l'atmosphère : étude de la réactivité du (beta)-pinène vis à vis des radicaux hydroxyles ; cas de la réactivité en milieu hétérogène." Université Joseph Fourier (Grenoble), 1995. http://www.theses.fr/1995GRE10129.

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L'objectif de ce travail etait d'etudier la photodegradation du beta-pinene, composeorganique volatil biogenique, en presence de radicaux hydroxyles et de determiner l'impact de particules solides sur cette photodegradation. Des artefacts analytiques ont ete rencontres lors de la mise au point du protocole de prelevement et d'analyse, et provenaient de la degradation de l'espece organique sur le support de prelevement pendant la thermodesorption. L'application d'un calcul correctif a permis de minimiser les erreurs d'artefact. Les etudes cinetiques effectuees sur les experiences en milieu homogene et en milieu heterogene, n'ont pas mis en evidence d'influence significative des particules sur la constante cinetique de reaction du beta-pinene. Toutefois, l'identification des produits secondaires a montre des differences notables entre les deux types de simulation. Dans nos conditions experimentales, des reactions d'oxydation heterogene apparaissent en presence de particules, mais ces mecanismes heterogenes sont negligeables d'un point de vue cinetique par rapport aux processus homogenes impliquant les radicaux hydroxyles
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45

Thompson, Michael George. "Hematin-catalyzed oxidation of linoleate as influenced by [beta]-casein." 1985. http://catalog.hathitrust.org/api/volumes/oclc/12812541.html.

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Thesis (M.S.)--University of Wisconsin--Madison, 1985.
Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 76-88).
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46

Richmond, Todd A. "A defect in beta-oxidation causes abnormal inflorescence development in Arabidopsis." 1997. http://catalog.hathitrust.org/api/volumes/oclc/39802233.html.

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Thesis (Ph. D.)--University of Wisconsin--Madison, 1997.
Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 171-183).
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47

Kunz, Hans-Henning [Verfasser]. "Biochemische Charakterisierung der Fettsäure-β-Oxidation [Fettsäure-beta-Oxidation] als Teil des Dunkelstoffwechsels von Arabidopsis thaliana / vorgelegt von Hans-Henning Kunz." 2009. http://d-nb.info/1006696490/34.

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48

Delker, Carolin [Verfasser]. "Jasmonatbiosynthse in Arabidopsis thaliana : Charakterisierung der Allenoxidcyclase-Genfamilie und von Mutanten der Fettsäure-β-Oxidation [Fettsäure-beta-Oxidation] / von Carolin Delker." 2007. http://d-nb.info/990045900/34.

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49

Lyvers, Peffer Pasha A. "Unraveling the pathway of lipid oxidation in the young pig assessment of hepatic [beta]-oxidation and characterization of carnitine palmitoyltransferase I (CPT I) /." 2004. http://www.lib.ncsu.edu/theses/available/etd-09142004-195837/unrestricted/etd.pdf.

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50

Yatsynych, Oksana. "Revisão das características farmacológicas do Meldonium. Uso no desporto como doping." Master's thesis, 2018. http://hdl.handle.net/10316/82169.

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Abstract:
Dissertação de Mestrado em Medicina do Desporto apresentada à Faculdade de Medicina
O Meldonium é um análogo estrutural do precursor da Carnitina, cujo mecanismo principal é inibir a síntese da Carnitina que é um transportador de FA do citoplasma para o interior da mitocôndria, local onde estes são oxidados. O principal objetivo da ação do Meldonium é alteração o processo da produção de ATP da oxidação dos ácidos gordos (FA), que requer alto consumo de oxigênio, até à glicólise, que aumenta da eficiência da produção de ATP. Nos certos países, o Meldonium é utilizado na prática médica para a normalização de funcionamento das estruturas celulares expostas a falta de oxigenação e é indicado para fins terapêuticos nas doenças cardiovasculares, metabólicas, neurológicas, nos períodos pós-operatórios e no caso de síndrome de abstinência no alcoolismo crónico. Devido ao crescente número de evidências sobre o uso indevido no desporto, em 2015 o Meldonium entrou no Programa de Monitorização de WADA. Durante a realização de Jogos Europeus em Baku em 2015, foi realizada uma analise, que revelou o Meldonium em grande parte dos atletas. Em geral o Meldonium foi detectado em 15 modalidades de desporto das 21. Em 2016 o Meldonium foi incluído na Lista de substâncias e métodos proibidos em todos os períodos (dentro e fora de competições). O objetivo do trabalho foi analizar os dados científicos disponíveis sobre o Meldonium e tentar chegar a uma conclusão se a substância de fato tem um efeito estimulante no organismo humano.Os estudos que foram realizados sobre o Meldonium, não têm um alto nível de evidência e até esta altura não existem resultados que claramente confirmem ou neguem as propriedades do Meldonium como doping.
Meldonium is a structural analogue of the Carnitine precursor, whose main mechanism is to inhibit the synthesis of Carnitine, which is a carrier of FA from the cytoplasm into the mitochondria, where they are oxidized. The main objective of the action of Meldonium is to alter the ATP production process of fatty acid oxidation (FA), which requires high oxygen uptake to glycolysis, which increases the efficiency of ATP production.In certain countries, Meldonium is used in medical practice to normalize the functioning of cellular structures exposed to lack of oxygenation and is indicated for therapeutic purposes in cardiovascular, metabolic, neurological diseases in the postoperative periods and in the case of withdrawal syndrome not chronic alcoholism.Due to increasing evidence of misuse in sport, in 2015 Meldonium entered the WADA Monitoring Program. During the European Games in Baku in 2015, an analysis was performed, which revealed the Meldonium in 66 athletes of the 762 (8.7%) during and before the competitions and in 22 athletes (of which 13 winners) of the 662 (3 , 5%), who personally announced the use of Meldonium. In general, Meldonium was detected in 15 sports modalities of 21. In 2016, Meldonium was included in the List of prohibited substances and methods in all periods (inside and outside competitions). The objective of the study was to analyze the available scientific data on Meldonium and to try to reach a conclusion as to whether the substance actually has a stimulating effect on the human body. Studies that have been conducted on Meldonium do not have a high level of evidence and to date there are no results that clearly confirm or deny the properties of Meldonium as doping.
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