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Dissertations / Theses on the topic 'Mitochondrial reactive oxygen species'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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1

Logan, Angela. "Production of reactive oxygen species in mitochondria and mitochondrial DNA damage." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609201.

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2

Hurd, T. R. "Interactions between mitochondrial protein thiols and reactive oxygen species." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604824.

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This work investigates the reactions of proteins with ROS when mitochondria are exposed to H<sub>2</sub>O<sub>2</sub> or when they generate ROS endogenously. Using isolated mitochondria, those proteins that are particularly sensitive to low concentrations of H<sub>2</sub>O<sub>2</sub> and to ROS generated by the mitochondrial electron transport chain were first identified using a method called Redox-Difference Gel Electrophoresis (Redox-DIGE). Most redox sensitive thiol proteins identified by Redox-DIGE were involved either in fatty acid oxidation or in the regulation of the pyruvate dehydroge

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Li, Xinyuan. "Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/320473.

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Pharmacology<br>Ph.D.<br>Lysophosphatidylcholines (LPCs) are a class of pro-inflammatory lipids that play important roles in atherogenesis. LPC activates endothelial cells (ECs) to upregulate adhesion molecules, cytokines and chemokines, which is the initiation step of atherogenesis. However, the mechanisms underlying LPC-triggered EC activation are not fully understood. Previously considered as the toxic by-products of cellular metabolism, mitochondrial reactive oxygen species (mtROS) are recently found to directly contribute to both the innate and adaptive immune responses. Here we tested a

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Hinchy, Elizabeth. "How cellular ATP/ADP ratios and reactive oxygen species affect AMPK signalling." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270029.

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Mitochondria are key generators of cellular ATP, vital to complex life. Historically, mitochondrial generation of reactive oxygen species (ROS) was considered to be an unregulated process, produced by dysfunctional mitochondria. More recently, mitochondrial ROS generated by complex I, particularly by the process of reverse electron transfer (RET), has emerged as a potentially biologically relevant signal that is tightly-regulated and dependent on mitochondrial status. ROS production by RET is reported to play a role in the innate immune response and lifespan extension in fruit flies. One way i

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5

Collins, Yvonne. "Regulation of pyruvate dehydrogenase kinase 2 by mitochondrial reactive oxygen species." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708470.

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6

Sanusi, Morufat Olayide Abisola. "Mitochondrial reactive oxygen species signalling and vascular smooth muscle cell senescence." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37968.

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Ageing is a risk factor for the development of cardiovascular disease. In particular, senescent vascular smooth muscle cells (VSMCs) have been observed within atherosclerotic plaques. Oxidants are widely implicated in vascular ageing and cardiovascular disease with evidence of oxidative stress in cells undergoing senescence. Our previous data showed that Angiotensin II caused stress induced premature senescence (SIPS) in primary human VSMC via oxidant generation. Prevention of senescence with a mitochondria targeted antioxidant, Mito-TEMPO, suggested the mechanism was dependent on mitochondria

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7

Rogers, Kara Emilie. "Mitochondrial Antioxidants, Protection Against Oxidative Stress, and the Role of Mitochondria in the Production of Reactive Oxygen Species." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194490.

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Mitochondria serve as the major source of reactive oxygen species (ROS) production in cells resulting in antioxidant systems and cell signaling pathways that are unique to mitochondria. Thioredoxin-2 (Trx-2) is the mitochondrial member of the thioredoxin superfamily, and acts specifically to reduce the mitochondrial peroxidase, peroxiredoxin-3. It has been proposed that Trx-2 associates with cytochrome c, which functions in mitochondrial respiration and apoptosis. Homozygous Trx-2 deletion in mice is embryonic lethal and it is hypothesized here that Trx-2 lethality is caused by loss of mito

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8

Schwarzlander, Markus. "The Response to Mitochondrial Reactive Oxygen Species and Redox Status in Plants." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504582.

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9

Garlid, Anders Olav. "Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling?" PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1641.

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Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa, ADT and Garlid, KD. Am J Physiol 295, H874-82, 2008). Superoxide (O2•-), hydrogen peroxide (H2O2), and hydroxyl radical (HO•) have each been proposed as the signaling ROS but the identity of the ROS responsi

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10

Hansson, Anna. "Cellular responses to respiratory chain dysfunction /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-493-7/.

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11

Apostolova, Nadezda. "Mitochondrial role of Apoptosis-Inducing Factor (AIF): Oxidative Phosphorylation and Reactive Oxygen Species." Doctoral thesis, Universitat de València, 2008. http://hdl.handle.net/10803/9775.

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The apoptotic function of Apoptosis-inducing factor (AIF) is well documented in theliterature, but its physiological role in the mitochondrion is less certain. Using a smallinterfering RNA (siRNA) strategy, we studied whether modulation of AIF expression incultured cells influenced the production of reactive oxygen species (ROS). We foundthat siAIF-transfected cells had reduced AIF protein levels and this was paralleled by asignificant increase in ROS. We tested the generality of this response by using twodifferent human cell lines, the hepatoma cell line Hep3B and cervix carcinoma lineHeLa, a

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12

Maranzana, Evelina Susana Beatriz <1971&gt. "Mitochondrial respiratory supercomplex association limits production of reactive oxygen species from Complex I." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6601/.

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Evidence accumulated in the last ten years has demonstrated that a large proportion of the mitochondrial respiratory chain complexes in a variety of organisms is arranged in supramolecular assemblies called supercomplexes or respirasomes. Besides conferring a kinetic advantage (substrate channeling) and being required for the assembly and stability of Complex I, indirect considerations support the view that supercomplexes may also prevent excessive formation of reactive oxygen species (ROS) from the respiratory chain. Following this line of thought we have decided to directly investigate ROS

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Brouillette, Marc James. "Mechanical stimulation of cartilage induces mitochondrial reactive oxygen species production mediating metabolic responses." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/5428.

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This dissertation project is unique in that it seeks to link two historically independent concepts: mechanical loading of cartilage (1) induces reactive oxygen species (ROS) release from specific mitochondrial complexes, and (2) results in observable metabolic alterations. It is well known that ROS are released from certain loading conditions. It has also been shown that chondrocytes respond favorably to cyclic loading at moderate stresses, as determined metabolically by proteoglycan and collagen production. However, this study aims to demonstrate that these phenomena are interdependent, and i

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Liu, Bin. "P53 AND REACTIVE OXYGEN SPECIES: A CONVOLUTED STORY." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_theses/450.

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The tumor suppressor p53 has a close relation with reactive oxygen species (ROS). As an indispensable component of the cellular redox system, ROS not only have been established to be involved in p53-dependent apoptosis, but also regulate p53 activity. Recent studies revealed several novel actions of p53, such as transactivation of antioxidative proteins, mitochondria translocation and inhibition of glycolysis. The fate of cells where p53 signaling pathways are initiated is either survival or death. In this review, we examine the hypothesis that ROS regulate cell fate through p53, in a way that

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15

Yang, Wen. "Mitochondrial dysfunction and reactive oxygen species metabolism in the aging process of «Caenorhabditis elegans»." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94989.

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The nematode roundworm Caenorhabditis elegans has been extensively used to study the genetics of aging. The functions of many genes have been found to be able to affect this animal's lifespan. A large proportion of these genes are expressed in mitochondria, an organelle that plays important roles in energy metabolism and generates reactive oxygen species (ROS). These two characteristics of mitochondria have both been suggested to be crucial for lifespan determination. One hypothesis, called the oxidative stress theory of aging, proposes that high oxidative damage caused by ROS generated in mi

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Deng, Ying. "ROLE OF THE REACTIVE OXYGEN SPECIES PEROXYNITRITE IN TRAUMATIC BRAIN INJURY." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/667.

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Reactive oxygen species (ROS) is cytotoxic to the cell and is known to contribute to secondary cell death following primary traumatic brain injury (TBI). We described in our study that PN is the main mediator for both lipid peroxidation and protein nitration, and occurred almost immediately after injury. As a downstream factor to oxidative damage, the peak of Ca2+-dependent, calpainmediated cytoskeletal proteolysis preceded that of neurodegeneration, suggesting that calpain-mediated proteolysis is the common pathway leading to neuronal cell death. The time course study clearly elucidated the i

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Ash, Catherine Elizabeth. "Functional and molecular mechanisms underlying reduced mitochondrial reactive oxygen species generation under dietary restricted feeding conditions." Thesis, University of Liverpool, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494167.

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Dietary restriction (DR) across a wide phylogenetic range increases both mean and maximal lifespan by retarding the ageing process and delaying the onset and incidence of age-related pathologies. DR animals exhibit reduced tissue oxidative damage but anti-oxidant enzyme activities and other defence mechanisms against reactive oxygen species (ROS) are not consistently upregulated In such animals. As an alternative explanation ROS generation was Studied in isolated mitochondria from tissues of DR rats. About 90% of cellular ROS generation is thought to result from the single electron transfer to

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18

Raucci, Frank. "SPHINGOLIPID-INDUCED ACTIVATION OF THE VOLUME-SENSITIVE Cl− CURRENT IS MEDIATED BY MITOCHONDRIAL REACTIVE OXYGEN SPECIES." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/2016.

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Swelling-activated Cl− current (ICl,swell) is an outwardly-rectifying current that plays an important role in cardiac electrical activity, cellular volume regulation, apoptosis, and acts as a potential effector of mechanoelectrical feedback. Persistent activation of ICl,swell has been observed in a number of models of cardiovascular disease. Previously we showed that angiotensin II (Ang II), endothelin-1 (ET-1), endothelial growth factor receptor (EGFR), and reactive oxygen species (ROS) produced by NADPH oxidase (NOX) and mitochondria are involved in the activation of ICl,swell by both osmot

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19

Duca, Edward. "Invadolysin, a conserved lipid droplet-associated protease interacts with mitochondrial ATP synthase and regulates mitochondrial metabolism in Drosophila." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5562.

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Invadolysin (inv) is a member of the M8 class of zinc-metalloproteases and is conserved throughout metazoans. It is essential for development and invadolysin homozygous Drosophila mutants are third instar larval lethal. These larvae exhibit a reduced larval brain size and an absence of imaginal discs. Detailed analysis showed that inv mutants exhibit pleiotropic effects, including defects with chromosome architecture, cell cycle progression, spindle assembly, nuclear envelope dynamics, protein turnover and problems with germ cell migration. These findings indicated that Invadolysin must have a

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20

Heyno, Eiri. "Production of reactive oxygen species in plasma membranes, mitochondria and chloroplasts." Paris 11, 2009. http://www.theses.fr/2009PA112192.

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Les formes réactives de l’oxygène (FRO) ont été analysées dans différents compartiments cellulaires en utilisant des méthodes spectroscopiques (UV/VIS, fluorescence, infrarouge, résonance paramagnétique électronique). L’identité et les mécanismes catalytiques des enzymes qui produisent les FRO dans les membranes plasmiques (MP) et les mitochondries ont été étudiés, ainsi que le rôle protectif de l’oxydase terminale plastidiale (PTOX) des chloroplastes. Cd2+ s’est révélé être un inhibiteur de la NADPH oxydase des MP. In vivo Cd2+ inhibait la production extracellulaire de O2. - mais stimulait l’

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21

Kramer, Adam Hildyard. "An investigation of the role of mitochondrial STAT3 and modulation of Reactive Oxygen Species in adipocyte differentiation." Thesis, Rhodes University, 2014. http://hdl.handle.net/10962/54632.

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Stem cells have the ability to differentiate into a myriad of different cell types. The understanding of the differentiation process is of paramount importance if we are to use these cells in the lab as well as in therapeutics. Here, the levels and localization of the signal transducer and activator of transcription 3 (STAT3), with particular attention focused on the mitochondrial serine 727 phosphorylated form of STAT3 (pSTAT3S727) during differentiation, was investigated. Using the murine preadipocyte progenitor cell line 3T3-L1, as well as adipose derived human mesenchymal stem cells (HMSC-

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Costa, Rute Alves Pereira e. 1984. "Avaliação das funções mitocondriais de células deficientes na proteína XPC, envolvida na via de reparo por excisão de nucleotídeos (NER) = Evaluation of mitochondrial functions of XPC protein deficient cells, involved in nucleotide excision repair (NER) pathway." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311361.

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Orientadores: Nadja Cristhina de Souza Pinto, Anibal Eugenio Vercesi<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-24T01:38:55Z (GMT). No. of bitstreams: 1 Costa_RuteAlvesPereirae_D.pdf: 10770990 bytes, checksum: 08f31895722a5f60be02fcde15d3ea05 (MD5) Previous issue date: 2013<br>Resumo: Xeroderma Pigmentosum (XP) é uma doença rara, autossômica recessiva, caracterizada por fotossensibilidade, mudanças pigmentares, envelhecimento precoce da pele e incidência elevada de neoplasias de pele. XP é causada por mutações

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23

Ho, Hsiang-Ting. "The Role of Reactive Oxygen Species in Arrhythmogenicity of Cardiac Glycoside." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1373401702.

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Silva, José Pablo. "The pathophysiology of respiratory chain dysfunction /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-234-9/.

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25

Blein, Sophie. "Étude de la variabilité du génome mitochondrial comme facteur de susceptibilité au cancer du sein." Thesis, Lyon 1, 2014. http://www.theses.fr/2014LYO10240/document.

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Une large part de la composante génétique du risque de cancer du sein est encore inexpliquée. J'ai ainsi étudié dans quelle mesure les variants observés sur le génome mitochondrial pourraient en partie expliquer ce risque. En effet la mitochondrie, en tant que source d'énergie cellulaire, est un organite impliqué dans la synthèse des espèces oxygénées réactives ou radicaux libres, éléments contribuant à l'instabilité génomique et au développement tumoral. Un premier axe de recherche m'a conduit à étudier une interaction potentielle entre des variants du génome mitochondrial et du génome nucléa

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Zuo, Li. "Molecular Mechanisms of Stress-induced Reactive Oxygen Species Formation in Skeletal Muscle." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1038853894.

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27

Lucas, Stephen Marc. "Valproic Acid Leads to an Increase in ROS Generation by Inhibiting the Deacetylation of Mitochondrial SOD." BYU ScholarsArchive, 2020. https://scholarsarchive.byu.edu/etd/9247.

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Valproic Acid Promotes Acetylation of Superoxide Dismutase-2 During Neurogenesis. Valproic acid (VPA) is a known developmental toxicant associated with a high prevalence of neural tube defects (NTD). The mechanism of VPA-induced NTD is unclear, but oxidative stress may be implicated. To understand how embryotoxic oxidative stress may occur, we measured superoxide dismutase (SOD) activity following VPA treatment in the embryonic pluripotent P19 mouse carcinoma cell line. In undifferentiated P19 cultures treated with VPA (5 mM), dichlorofluorescein fluorescence increased 15% compared to untreate

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Bowling, Benjamin D. "Inhibition of mitochondrial protein translation sensitizes melanoma cells to arsenic trioxide cytotoxicity via a reactive oxygen species dependent mechanism." [New Haven, Conn. : s.n.], 2008. http://ymtdl.med.yale.edu/theses/available/etd-11212008-111938/.

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29

Barlow, Jonathan. "Mitochondrial involvement in pancreatic beta cell glucolipotoxicity." Thesis, University of Plymouth, 2015. http://hdl.handle.net/10026.1/3314.

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High circulating glucose and non-esterified free fatty acid (NEFA) levels can cause pancreatic β-cell failure. The molecular mechanisms of this β-cell glucolipotoxicity are yet to be established conclusively. In this thesis by exploring mitochondrial energy metabolism in INS-1E insulinoma cells and isolated pancreatic islets, a role of mitochondria in pancreatic β-cell glucolipotoxicity is uncovered. It is reported that prolonged palmitate exposure at high glucose attenuates glucose-stimulated mitochondrial respiration which is coupled to ADP phosphorylation. These mitochondrial defects coinci

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Julienne, Cloé Mimsy. "Altérations du métabolisme énergétique mitochondrial lors de la cachexie cancéreuse." Thesis, Tours, 2012. http://www.theses.fr/2012TOUR3318/document.

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La cachexie est un syndrome complexe caractérisé par une balance énergétique négative. Le rôle joué par le métabolisme énergétique mitochondrial dans ce syndrome est peu connu. Nos précédents travaux montraient une diminution de la synthèse de l’ATP dans les mitochondries hépatiques en stade de cachexie cancéreuse sévère. Dans ce travail, nous démontrons, in vitro, que l’augmentation de la production d’espèce réactive de l’oxygène et du contenu en cardiolipine dans des mitochondries hépatiques saines, mime partiellement les mécanismes observés lors d’un stade cachexie sévère. Nous observons ce

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Lashin, Ossama M. "Functional modification of cardiac mitochondria in type-I diabetes." Connect to text online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1093467515.

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Thesis (Ph. D.)--Case Western Reserve University, 2005.<br>[School of Medicine] Department of Physiology and Biophysics. Includes bibliographical references. Available online via OhioLINK's ETD Center.

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Barnes, Robert. "A nuclear role for the respiratory enzyme CLK-1 in regulating reactive oxygen species, the mitochondrial unfolded protein response and longevity." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/a-nuclear-role-for-the-respiratory-enzyme-clk1-in-regulating-reactive-oxygen-species-the-mitochondrial-unfolded-protein-response-and-longevity(9a41f8d6-d11d-4102-b250-7b20091f4ded).html.

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As the major source of energy in the cell, mitochondria need to be able to effectively communicate their status to the nucleus. Defects in this process can have profound effects on the health of an organism and may affect its lifespan. The mitochondrial enzyme CLK-1 is required to produce ubiquinone for respiration and CLK-1 loss of function mutants have been shown to increase lifespan in both Caenorhabditis elegans and mammals. In this thesis, it is demonstrated that in addition to its mitochondrial role, CLK-1 also localises to the nucleus in C. elegans. This nuclear localisation is mediated

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MacLellan, James Darcy. "Effects of the mitochondrial uncoupling protein 3 on fuel substrate oxidation and reactive oxygen species formation in rat L6 muscle cells." Thesis, University of Ottawa (Canada), 2007. http://hdl.handle.net/10393/27533.

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Uncoupling protein 3 (UCP3) is an integral mitochondrial membrane protein thought to disassociate fuel substrate oxidation by allowing proton re-entry into the mitochondrial matrix. Expression of UCP3 has been correlated with fatty acid and glucose metabolism, and reactive oxygen species (ROS) formation. To improve our understanding of the potential involvement of UCP3 in such pathways we investigated the effects of a UCP3 overexpression (2.2-2.5 fold) in the L6 muscle cell line. These findings were compared to those of UCP2 overexpression and DNP exposure. Palmitate oxidation was significantl

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Endoh, Yasumi Medical Sciences Faculty of Medicine UNSW. "New mechanisms modulating S100A8 gene expression." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/42942.

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S100A8 is a highly-expressed calcium-binding protein in neutrophils and activated macrophages, and has proposed roles in myeloid cell differentiation and host defense. Functions of S100A8 are not fully understood, partly because of difficulties in generating S100A8 knockout mice. Attempts to silence S100A8 gene expression in activated macrophages and fibroblasts using RNA interference (RNAi) technology were unsuccessful. Despite establishing validated small interfering RNA (siRNA) systems, enzymaticallysynthesized siRNA targeted to S100A8 suppressed mRNA levels by only 40% in fibroblasts activ

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Herb, Marc [Verfasser], Björn [Gutachter] Schumacher, and Martin [Gutachter] Krönke. "Mitochondrial reactive oxygen species license pro-inflammatory signaling in infected macrophages via disulfide linkage of NEMO / Marc Herb ; Gutachter: Björn Schumacher, Martin Krönke." Köln : Universitäts- und Stadtbibliothek Köln, 2019. http://d-nb.info/1178671852/34.

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Jang, Kyoung-Jin. "Mitochondrial function provides instructive signals for activation-induced B cell fates." Kyoto University, 2015. http://hdl.handle.net/2433/199208.

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Merabet, Nadège. "Modélisation mathématique de la production d'espèces actives de l'oxygène par la chaîne respiratoire mitochondriale : vers une meilleure compréhension de l'atrophie optique dominante de type 1." Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30026.

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L’ATP est synthétisée par les mitochondries à partir de réactions d’oxydoréduction catalysées les complexes de la chaîne respiratoire. Ces réactions impliquent des transferts d’électrons intra-protéine. Une capacité de production de l’anion superoxyde, formé par la réaction de l’oxygène avec un électron, a été identifiée pour les complexes I et III. Les espèces actives de l’oxygène (EAOs) sont des molécules dérivées de l’anion superoxyde. Si elles ne sont pas correctement régulées par les défenses antioxydantes de la cellule, ces EAOs peuvent réagir avec les composants de la cellule et nuire à

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Belikov, Aleksey Vitalyevich [Verfasser], and Luca [Akademischer Betreuer] Simeoni. "The role of reactive oxygen species and mitochondria in T-cell activation / Aleksey Vitalyevich Belikov. Betreuer: Luca Simeoni." Magdeburg : Universitätsbibliothek, 2016. http://d-nb.info/1100055479/34.

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Desmoulins, Lucie. "Détection hypothalamique du glucose chez le rat soumis à un régime gras enrichi en saccharose : rôle de la dynamique mitochondriale et des espèces actives de l'oxygène d'origine mitochondriale." Thesis, Dijon, 2016. http://www.theses.fr/2016DIJOS024/document.

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L’hypothalamus participe au contrôle de l’homéostasie énergétique en détectant les signaux circulants tels que le glucose. L’hypothalamus médiobasal (MBH) en particulier, est capable de détecter l’hyperglycémie afin d’initier des réponses physiologiques adaptées, comme par exemple la sécrétion d’insuline via le système nerveux autonome (par un contrôle vagal). Notre équipe a récemment montré que la détection du glucose nécessite la production d’espèces actives de l’oxygène d’origine mitochondriale (mROS), fortement dépendante de la dynamique mitochondriale (fusion et fission). Récemment, l’étu

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Aitken, Gillian Roxburgh. "Investigation of UV-induced reactive oxygen and nitrogen species in human skin cells and its association with the individual complexes of the mitochondrial electron transport chain." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424156.

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Bagsiyao, Pamela. "Role of brain uncoupling proteins in energy homostasis and oxygen radical metabolism." Honors in the Major Thesis, University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/1025.

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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.<br>Bachelors<br>Burnett College of Biomedical Sciences<br>Molecular Biology and Microbiology

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Dehina, Leila. "Influence de l’ischémie et de la cinétique de reperfusion myocardique sur la structure et le fonctionnement des mitochondries chez le porc : effets de la trimétazidine, de la ranolazine et du propranolol." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10006.

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La production de radicaux libres oxygénés (ROS), la surcharge calcique cytosolique et l’ouverture des pores de transition membranaires mitochondriales (mPTP) consécutives à l’ischémie myocardique (IM) sont aggravées lors de la reperfusion. Dans cette thèse, nous nous sommes intéressés : 1) à l’évaluation des effets de la trimétazidine sur le seuil électrique de fibrillation ventriculaire (VFT) et sur les lésions structurales et fonctionnelles des mitochondries lors de l’IM (étude 1, N=26 porcs); 2) à la détermination de la cinétique d’évolution des lésions d’ischémie/reperfusion (I/R) (étude 2

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Pan, Minglin, Ying Han, Rui Si, Rui Guo, Ankit Desai, and Ayako Makino. "Hypoxia-induced pulmonary hypertension in type 2 diabetic mice." SAGE PUBLICATIONS INC, 2017. http://hdl.handle.net/10150/623894.

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Hypoxia-induced pulmonary hypertension (HPH) is a progressive disease that is mainly caused by chronic exposure to high altitude, chronic obstructive lung disease, and obstructive sleep apnea. The increased pulmonary vascular resistance and increased pulmonary arterial pressure result in increased right ventricular afterload, leading to right heart failure and increased morbidity. There are several clinical reports suggesting a link between PH and diabetes, insulin resistance, or obesity; however, it is unclear whether HPH is associated with diabetes as a progressive complication in diabetes.

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Savu, Octavian. "Mechanisms of chronic complications of diabetes with focus on mitochondria and oxygen sensing." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-764-1/.

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Giedt, Randy James. "Real-Time Acquisition and Analysis of Endothelial Mitochondrial Superoxide Radical Production and Membrane Potential During In Vitro Ischemia/Reperfusion." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243541457.

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Giedt, Randy James. "Mitochondrial Network Dynamics in Vascular Endothelial Cells Exposed to Mechanochemical Stimuli: Experimental and Mathematical Analysis." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1333985787.

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Semont, Audrey. "Implication des ROS mitochondriaux dans le couplage excitation contraction cardiaque." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0426.

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L’activation électrique des cardiomyocytes, via le courant de dépolarisation qu’elle induit, est primordiale dans la contraction cardiaque qui requiert l’adéquation de la production d'énergie par les mitochondries et des besoins énergétiques de l’appareil contractile. Les espèces radicalaires de l'oxygène (ROS) ont été récemment impliquées dans la régulation de nombreux acteurs du couplage excitation-contraction cardiaque. L’objectif de ce travail est d’explorer l'implication des ROS d'origine mitochondriale dans la régulation du couplage excitation-contraction au niveau du cardiomyocyte, en c

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Assaly, Rana. "Protection du myocarde ischémique et pore géant mitochondrial : applications pharmacologiques." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00734466.

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La maladie coronaire d'origine ischémique reste l'une des principales causes de mortalité dans le monde industrialisé. Le traitement de l'ischémie aiguë du myocarde est cependant entré dans une nouvelle ère où la mortalité peut être diminuée de moitié en utilisant des procédures qui permettent un retour rapide du débit sanguin dans la zone ischémique du myocarde, c'est-à-dire la revascularisation. Toutefois, cette reperfusion entraîne par elle-même des complications appelées lésions de la reperfusion qui ont été décrites pour la première fois par Jennings et al., en 1960. Par conséquent, le dé

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Silva, Carolina Solon da 1982. "Apoptose induzida por palmitato em células HEPG2 depende da produção de TNF-Alfa." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309382.

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Orientador: Gabriel Forato Anhê<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-21T11:57:04Z (GMT). No. of bitstreams: 1 Silva_CarolinaSolonda_M.pdf: 587503 bytes, checksum: cd74a1063d709369d29c9a998e1cc9a4 (MD5) Previous issue date: 2012<br>Resumo: A prevalência de esteato hepatite não alcólica (NASH) aumenta de 20% em indivíduos magros para 80% em pacientes obesos com inflamação hepática caracterizada por elevados níveis de TNF-alfa. Um dos eventos que caracteriza a evolução para NASH é a marcante morte de

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Semete, Boitumelo. "Analysis of metallothionein gene expression in oxidative stress related disorders / by Boitumelo Semete." Thesis, North-West University, 2004. http://hdl.handle.net/10394/51.

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Increased reactive oxygen species (ROS) have been reported to be at the centre of various diseases. Although several reports have implicated elevated levels of ROS in the pathogenesis of diabetes mellitus, the early detection of ROS is still not attainable. This limitation causes difficulty in the early diagnosis of ROS related disorders. The presence of high levels of ROS was reported to result in differential expression of antioxidant genes involved in protecting cells from their deleterious effects. Among the antioxidant genes that are expressed, it was postulated that expression of metallo

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