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Smith, Cheryl. "Reactive oxygen species in atherosclerosis". Thesis, King's College London (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302549.
Pełny tekst źródłaStanczak, Anna. "Reactive oxygen species in laundry applications". Thesis, Durham University, 2018. http://etheses.dur.ac.uk/12885/.
Pełny tekst źródłaWu, Wan Man. "Reactive oxygen species and murine malaria". Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26446.
Pełny tekst źródłaYu, Tian-Wei. "Genotoxic damage induced by reactive oxygen species". Thesis, University of Surrey, 1997. http://epubs.surrey.ac.uk/764/.
Pełny tekst źródłaBaumber, Julie. "Reactive oxygen species and equine sperm function /". For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.
Pełny tekst źródłaXie, Ruiyu. "Reactive Oxygen Species-Induced Necrotic Cell Death". Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195215.
Pełny tekst źródłaCowgill, Danielle Lee. "FIELD DECTION DEVICE OF REACTIVE OXYGEN SPECIES". DigitalCommons@CalPoly, 2013. https://digitalcommons.calpoly.edu/theses/1107.
Pełny tekst źródłaYamamoto, Shinichiro. "Reactive Oxygen Species / Reactive Nitrogen Species-sensitive TRP channels : Molecular Activation Mechanism and Physiological Significance". 京都大学 (Kyoto University), 2008. http://hdl.handle.net/2433/124503.
Pełny tekst źródłaLiu, Bin. "P53 AND REACTIVE OXYGEN SPECIES: A CONVOLUTED STORY". UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_theses/450.
Pełny tekst źródłaLloyd, Daniel Robert. "Formation of DNA damage by reactive oxygen species". Thesis, Institute of Cancer Research (University Of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298187.
Pełny tekst źródłaMian, Kousar Bashir. "Inhibition of nitric oxide by reactive oxygen species". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318114.
Pełny tekst źródłaPinto, Ana Filipa Carapinha. "Reductive scavenging of reactive oxygen species in prokaryotes". Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2012. http://hdl.handle.net/10362/9918.
Pełny tekst źródłaThe purpose of this thesis is to contribute to a better understanding of systems involved in the scavenging of reactive oxygen species. The work focuses on an enzyme from the Rubrerythrin family that reduces hydrogen peroxide and one from the Superoxide Reductase family that reduces the superoxide anion. Both of these families are distributed widely across the three domains of life, Archaea, Bacteria and Eukarya, but are mainly found in anaerobic and microaerophilic prokaryotes.(...)
Bustami, Mona Ratib. "Reactive oxygen and nitrogen species in cystic fibrosis". Thesis, University of Bath, 2002. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248100.
Pełny tekst źródłaSoltau, Carl Peter. "Nitroxide trapping of radical species formed from the reaction of sulfoxides with reactive oxygen species". Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/210339/1/Carl_Soltau_Thesis.pdf.
Pełny tekst źródłaSun, Zhenning. "Studies on fluorescent probes for the specific detection of reactive oxygen species and reactive nitrogen species in living cells". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36845395.
Pełny tekst źródłaHole, Paul Spencer. "Role of reactive oxygen species in ras-mediated leukaemogenesis". Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54355/.
Pełny tekst źródłaHurd, 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.
Pełny tekst źródłaCetinbas, Naniye. "Reciprocal regulation of glutamine metabolism and reactive oxygen species". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45714.
Pełny tekst źródłaTatla, Sangeeta. "The role of reactive oxygen species in lymphocyte activation". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244071.
Pełny tekst źródłaZeng, Zhen [Verfasser], Albert [Akademischer Betreuer] Gollhofer i Daniel [Akademischer Betreuer] König. "Effects of dietary strategies on reactive oxygen species production". Freiburg : Universität, 2021. http://d-nb.info/1237617979/34.
Pełny tekst źródłaFisher, Helen M. "Mechanisms of reactive oxygen species generation by mammalian spermatozoa". Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20503.
Pełny tekst źródłaArellanes, Chuautemoc. "Measurements of reactive oxygen species in the particle phase". Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1679290751&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Pełny tekst źródłaSun, Zhenning, i 孫振宁. "Studies on fluorescent probes for the specific detection of reactive oxygen species and reactive nitrogen species in living cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38677490.
Pełny tekst źródłaMallon, P. T. "The modulation of experimental colitis by reactive oxygen species scavengers". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484983.
Pełny tekst źródłaSand, Carsten. "Pharmacological investigations on reactive oxygen species in the cardiovascular system". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2002. http://dare.uva.nl/document/64883.
Pełny tekst źródłaEdmonds, Sally Elizabeth. "Hypoxia and reactive oxygen species : therapeutic implications for rheumatoid synovitis". Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286596.
Pełny tekst źródłaRahman, Mashrur. "Reactive oxygen species mediated regulation of autophagy in skeletal muscles". Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121322.
Pełny tekst źródłaLes muscles squelettiques constituent environ 50% de la masse du corps humain et représente un organe essentiel permettant la locomotion et le contrôle métabolique. L'autophagie, un processus catabolique lysosome-dépendant, est impliquée dans la dégradation des protéines et des organites à long terme. Elle représente un processus important pour le maintien de l'homéostasie du muscle. Par ailleurs, il a été montré que les radicaux libres (ROS) principalement générés par les mitochondries, induisent l'autophagie dans de nombreux types cellulaires. Dans cette étude, nous voulons évaluer des radicaux libres mitochondriaux (ROS) à un niveau physiologique sur l'autophagie dans le muscle squelettiqueDans les myotubes différenciés C2C12, le niveau basal de l'autophagie et son activation (déclenchées par 1,5 à 4 h de carence aigüe en nutriments, par l'inhibition de mTORC1, ou encore par la privation en leucine) ont été quantifiés à l'aide d'un test de longue durée de dégradation des protéines (indice de protéolyse), par le flux d'autophagie LC3B, ou par les l'ARNm des gènes liés à l'autophagie. La pré-incubation avec des antioxydants de type tempol (SOD mimétique) ou N-acétylcystéine (NAC) atténue considérablement les niveaux de protéolyse, de flux de LC3B et bloque l'activation de l'autophagie secondaire à la carence en nutriments –traitement par rapamycine- ou la carence en leucine. Des résultats similaires ont été obtenus avec es antioxydants spécifiques de la mitochondrie mito-tempol et SS31. Des mesures de fluorescence rouge MitoSOXTM confirment que le niveau de radicaux libres mitochondriaux augmentent considérablement en réponse à une carence en nutriments aiguë ou au traitement par rapamycine et que le tempol et mito-tempol atténue cette réponse. Les antioxydants entraîne une diminution de 40% de la phosphorylation de l'AMPK et augmente significativement la phosphorylation de l'AKT, mais sans exercer aucun effet sur mTORC1 qui est dépendant de la phosphorylation sur Ser555 ULK1. Le traitement des souris avec NAC atténue significativement le flux autophagique basal de LC3B dans le diaphragme, ce qui confirme que les ROS endogènes favorise l'autophagie musculaire in vivo.Nous rapportons pour la première fois que les ROS mitochondriaux sont responsable de l'activation de l'autophagie dans le muscle squelettique et que cet effet est médié en partie par l'inhibition de AKT et de l'initiation de l'autophagie par activation de l'AMPK.
Wolfe, James T. "A role for reactive oxygen species in apoptotic cell death". Thesis, University of Leicester, 1996. http://hdl.handle.net/2381/34277.
Pełny tekst źródłaPerkins, Talayia Nayette. "The effect of reactive oxygen species on aged skeletal muscle". Thesis, Virginia Tech, 1997. http://hdl.handle.net/10919/46503.
Pełny tekst źródłaMaster of Science
Zhu, Haizhou. "Novel Reactive Oxygen Species Activated Scaffold from Mechanism to Application". University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1573811146199126.
Pełny tekst źródłaLi, 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.
Pełny tekst źródłaPh.D.
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 novel hypothesis that mtROS serve as signaling mediators for LPC-induced EC activation. Using electron spin resonance and flow cytometry with mtROS-specific fluorescence probe MitoSOX, we found that several LPC species including LPC 16:0, 18:0, and 18:1 induced mtROS in human primary aortic ECs (HAECs). Mechanistically, our analysis using confocal microscopy and Seahorse XF96 mitochondrial function analyzer showed that LPC induced mtROS via increasing mitochondrial calcium-mediated increase of mitochondrial respiration. In addition, we found that mtROS scavenger MitoTEMPO abolished LPC-induced EC activation by downregulating Intercellular adhesion molecule 1 (ICAM-1) in HAECs. Moreover, our analysis with mass spectrometer analysis of histone H3 lysine acetylation and electrophoretic mobility shift assay (EMSA) showed that MitoTEMPO acts by blocking LPC-induced histone H3 lysine 14 acetylation (H3K14ac) and nuclear translocation of pro-inflammatory transcription factor activator protein-1 (AP-1). Remarkably, all the above effects can be inhibited by anti-inflammatory cytokines interleukin (IL-35) and IL-10. Our results indicate that mtROS are responsible for LPC-induced EC activation, which can be inhibited by anti-inflammatory cytokines. MtROS targeting therapies and anti-inflammatory cytokines such as IL-35 may serve as novel therapeutic targets for vascular inflammation and cardiovascular diseases. The studies in this dissertation were supported by grants from the National Institutes of Health (NIH) funded to Dr. Xiao-Feng Yang.
Temple University--Theses
Al-Nu'airat, Jomana. "Implications of reactive oxygen species (ROS) in initiating chemical reactions". Thesis, Al-Nu'airat, Jomana (2018) Implications of reactive oxygen species (ROS) in initiating chemical reactions. PhD thesis, Murdoch University, 2018. https://researchrepository.murdoch.edu.au/id/eprint/42916/.
Pełny tekst źródłaWinkler, Jonathan Alexander. "Improving antibiotic activity by manipulating bacterial reactive oxygen species metabolism". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12675.
Pełny tekst źródłaThe discovery of antibiotics was one of the most important medical breakthroughs of the twentieth century, having a broad impact on overall life expectancy and public health. Unfortunately, antibiotic discovery has slowed significantly in recent times and has failed to match the rising incidence of antibiotic-resistant pathogens. Gram-negative pathogens are a particularly troublesome threat, primarily because these bacteria possess an outer membrane that prevents many antibiotics from accessing their primary cellular targets. While the discovery of novel antibiotics could help to address these issues, alternative strategies, such as improving the activity of preexisting antibiotics, are also needed. Bactericidal antibiotics have recently been shown to share a common mechanism of cell death, despite having different primary, cellular targets. This shared mechanism involves the metabolic production of reactive oxygen species (ROS), which can damage proteins, lipids, and nucleic acids, and can ultimately result in bacterial cell death. The body of work described here shows that this common mechanism can be exploited to improve antibiotic activity, regardless of the antibiotic's primary mode of action. First, I will describe how bacterial metabolism can be predictably perturbed to increase endogenous ROS production, and that increasing endogenous ROS is sufficient to enhance bacterial sensitivity to treatments with ROS-generating biocides, antibiotics, and immune cell attack. I will then describe work indicating that an ancient antimicrobial agent, silver salts, can also increase endogenous ROS production and potentiate the activity of multiple antibiotic classes. Furthermore, I show that silver salts can increase the outer membrane permeability of a Gram-negative organism. This property is exploited to enable vancomycin, an antibiotic that is specific for Gram-positive bacteria, to work against a Gram-negative organism. Together, this body of work demonstrates that bacterial ROS metabolism can be exploited effectively to enhance. antibiotic activity, which ultimately could result in the discovery and development of novel antimicrobial agents.
Hecht, castro medeiros Fabio. "The role of reactive oxygen species in thyroid radio-carcinogenesis". Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS085.
Pełny tekst źródłaPapillary thyroid cancers (PTC) are the most common endocrine tumors and account for 2-3% of all human cancers. The most relevant genetic alterations found in these tumors are mutations in the genes BRAF and RAS, and chromosomal translocations in RET, a proto-oncogene activated in 15-20% of PTCs. These oncogenic translocations, known as RET/PTCs, result from the fusion of RET with unrelated partner genes. Ionizing radiation is a major risk factor for RET/PTC formation, however, the molecular mechanisms involved in these radioinduced translocations just begun to be unveiled. In the past few years, our group has reported a critical role for reactive oxygen species (ROS) in the formation of RET/PTC in thyroid cells in vitro and has also shown that irradiation can elicit a persistent oxidative stress caused by the upregulation of the NADPH Oxidase DUOX1 that leads to DNA damage, mediating at least part of the effects of radiation. However, how could ROS lead to the formation of RET/PTC is not fully understood. Children are at significantly higher risk of developing radio-induced thyroid tumors, specially RET/PTC positive, probably due to the intense proliferation rate of their follicular thyroid cells. This epidemiological observation prompts the assumption that replication dynamics may be involved in RET/PTC formation. Indeed, it has been shown that the pharmacological induction of replicative stress can stimulate the in vitro formation of RET/PTC in thyroid cells. Thus, to investigate whether replicative stress might contribute for the long-term effects of irradiation on DNA damage and RET/PTC formation, we analyzed the effects of radiation in NTHY-ori3.1 thyroid cell lineage in terms of oxidative and replicative stress and replication dynamics. Our results confirm that irradiation triggers two waves of oxidative stress: first, a strong but transient oxidative burst takes place minutes after irradiation and next, a persistently increased oxidative stress that starts only 2 days after irradiation. These two peaks of oxidative stress lead to two peaks of DNA damage. Irradiation caused little or no effect on proliferation nor on cell cycle progression. However, several protein markers of replicative stress, such as pATR, pATM, pChk1 and pRPA are induced three days after irradiation. Moreover, replication dynamics analysis revealed a diminished replication speed that has been reversed by antioxidants, suggesting that oxidative stress may contribute to replication defects. Finally, using ChIP-qPCR, we observed that the genes involved in RET/PTC1 translocation present more double-stranded breaks than RET/PTC-unrelated genes 3 days after irradiation. Hence, we propose that replicative stress is potentially involved in the etiology of RET/PTC-positive tumors
HECHT, Fabio. The role of reactive oxygen species in thyroid radio-carcinogenesis. Rio de Janeiro, 2018. Doctoral thesis - Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil and Université Paris-Saclay, Orsay, France, 2018.O câncer papilífero de tireoide é o tumor endócrino mais comum e corresponde a 2-3% de todos os cânceres humanos. As alterações genéticas mais relevantes relacionadas a esse tumor são mutações nos genes BRAF e RAS e translocações do gene RET, um proto-oncogene ativado em 15-20% dos tumores papilíferos. Essas translocações, conhecidas como RET/PTC, resultam da fusão de RET com diversos outros genes. A radiação ionizante é um importante fator de risco para a formação de RET/PTC, no entanto, o mecanismo molecular responsável por essa translocação radioinduzida ainda não foi elucidado. Nos últimos anos, nosso grupo demonstrou um papel crítico exercido pelas espécies reativas de oxigênio na formação de RET/PTC em células tireoidianas in vitro e também mostrou que a irradiação promove um estresse oxidativo persistente causado pelo aumento de expressão da NADPH Oxidase DUOX1, levando à dano ao DNA, mediando assim parte dos efeitos da radiação. No entanto, como o ROS leva à formação de RET/PTC ainda não é compreendido. Crianças possuem um risco significativamente mais alto de desenvolver tumores tireodianos após a irradiação, especialmente RET/PTC positivos, provavelmente em função da intensa proliferação das células tireodianas. Essa associação sugere que a replicação esteja envolvida na formação de RET/PTC. De fato, foi observado que a indução farmacológica de estresse replicativo pode estimular a formação in vitro de RET/PTC em células tireodianas. Portanto, para investigar se o estresse replicativo contribui com os efeitos da irradiação no longo prazo sobre o dano ao DNA e formação de RET/PTC, nós investigamos o papel da radiação sobre o estresse oxidativo e replicativo, além da dinâmica de replicação de linhagem de células tireodianas NTHY-ori 3.1. Nossos resultados confirmam que a irradiação desencadeia duas ondas de estresse oxidativo: primeiramente, um forte, mas transitório pico de espécies reativas de oxigênio é observado minutos após a irradiação, seguido por um novo e persistente pico que só é observado a partir de dois dias após a irradiação. Esses dois picos de estresse oxidativo resultam em dois picos de dano ao DNA. A irradiação causou pouco ou nenhum efeito na proliferação ou na progressão do ciclo celular. No entanto, vários marcadores de estresse replicativo foram observados três dias após a irradiação, como pATR, pATM, pChk1 e pRPA. Além disso, a análise da dinâmica de replicação mostrou uma diminuição na velocidade da replicação que foi revertida por antioxidantes, sugerindo que o estresse oxidativo contribui para distúrbios dos mecanismos replicativos. Por fim, utilizando ChIP-qPCR, nós observamos que os genes envolvidos na translocação RET/PTC possuem mais quebras duplas do que genes endógenos, dias após a irradiação. Portanto, propomos que o estresse replicativo está potencialmente envolvido na etiologia dos tumores RET/PTC positivos
Rizzo, Benedetta <1987>. "Role of Reactive Oxygen Species in signalling and oxidative stress". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6966/1/Benedetta_Rizzo_PhD.pdf.
Pełny tekst źródłaRizzo, Benedetta <1987>. "Role of Reactive Oxygen Species in signalling and oxidative stress". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2015. http://amsdottorato.unibo.it/6966/.
Pełny tekst źródłaKing, Caitriona Maria. "An investigation of antioxidant status DNA repair capability and mutation as a function of age in humans". Thesis, University of Ulster, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390064.
Pełny tekst źródłaLi, Jian-Mei. "Molecular structure and biochemical properties of an endothelial cell NADP oxidase". Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272282.
Pełny tekst źródłaKafentzi, Maria Chrysanthi. "Reactive copper-oxygen species for C-H activation : influence of nuclearity and oxygen atom donor". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4355/document.
Pełny tekst źródłaCopper-containing monooxygenases are enzymatic systems capable of transferring an oxygen atom to their subtrates in highly regio or stereo-specific modes. Model complexes for copper-containing monooxygenases have provided valuable information on the structure and reactivity of several copper-dioxygen adducts. However, the recent discovery of two new enzymatic systems (LPMO and pMMO) able to perform activation of very strong C-H bonds has re-opened the debate on the catalytically relevant copper-dioxygen species. The use of model systems that mimic an enzyme is a simple approach to obtain a better knowledge of how nature works. For this study, Cu(I) and Cu(II) complexes containing ligand-substrate were prepared. After reaction with different oxidants or O-atom donors, we investigated the regio- and stereo-selectivity of the oxidation of the internal substrate. Based on the relatively well-known chemistry of Cu(I) with dioxygen, we, were also interested in investigating the water as an O-atom donor in C-H bond activation reactions. We have therefore investigated electrochemical water oxidation or activation to generate dioxygen and selective oxygen-insertion into the substrate-bound moiety. Finally, we explored the properties of mixed-metal dioxygen species as compared to their homometalic counter-parts. Indeed heterobimetallic active sites are found in various metalloenzymes such as cytochrome c oxidase. Therefore, two new high-valent Cu-Ni heterobimetallic complexes were synthesized. We investigated their electronic properties using various spectroscopic methods and their reactivity was evaluated towards external and internal substrates (indane)
Kafentzi, Maria Chrysanthi. "Reactive copper-oxygen species for C-H activation : influence of nuclearity and oxygen atom donor". Electronic Thesis or Diss., Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4355.
Pełny tekst źródłaCopper-containing monooxygenases are enzymatic systems capable of transferring an oxygen atom to their subtrates in highly regio or stereo-specific modes. Model complexes for copper-containing monooxygenases have provided valuable information on the structure and reactivity of several copper-dioxygen adducts. However, the recent discovery of two new enzymatic systems (LPMO and pMMO) able to perform activation of very strong C-H bonds has re-opened the debate on the catalytically relevant copper-dioxygen species. The use of model systems that mimic an enzyme is a simple approach to obtain a better knowledge of how nature works. For this study, Cu(I) and Cu(II) complexes containing ligand-substrate were prepared. After reaction with different oxidants or O-atom donors, we investigated the regio- and stereo-selectivity of the oxidation of the internal substrate. Based on the relatively well-known chemistry of Cu(I) with dioxygen, we, were also interested in investigating the water as an O-atom donor in C-H bond activation reactions. We have therefore investigated electrochemical water oxidation or activation to generate dioxygen and selective oxygen-insertion into the substrate-bound moiety. Finally, we explored the properties of mixed-metal dioxygen species as compared to their homometalic counter-parts. Indeed heterobimetallic active sites are found in various metalloenzymes such as cytochrome c oxidase. Therefore, two new high-valent Cu-Ni heterobimetallic complexes were synthesized. We investigated their electronic properties using various spectroscopic methods and their reactivity was evaluated towards external and internal substrates (indane)
Jiang, Hong 1964 Dec 6. "Role of reactive oxygen species on mouse sperm hyperactivation and capacitation". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22744.
Pełny tekst źródłaDíaz, Albíter Héctor Manuel. "Reactive oxygen species and antioxidant enzymes in the Lutzomyia-Leishmania system". Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569775.
Pełny tekst źródłaXiong, Yiqin. "ROLE OF REACTIVE OXYGEN SPECIES PEROXYNITRITE IN TRAUMATIC SPINAL CORD INJURY". UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/657.
Pełny tekst źródłaDeng, Ying. "ROLE OF THE REACTIVE OXYGEN SPECIES PEROXYNITRITE IN TRAUMATIC BRAIN INJURY". UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/667.
Pełny tekst źródłaGapper, Catherine Lucia. "Roles and Regulation of Reactive Oxygen Species Involved in Cell Growth". Thesis, University of East Anglia, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502509.
Pełny tekst źródłaGiurnazi, Ali Mansour. "Involvement of reactive oxygen species generation in cellular and subcellular fractions". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318298.
Pełny tekst źródłaD'Souza, Richard Joseph. "The importance of reactive oxygen species in determining mesangial cell growth". Thesis, St George's, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283240.
Pełny tekst źródłaMuzaffar, Saima. "Reactive oxygen species and the pathophysiology of adult respiratory distress syndrome". Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271916.
Pełny tekst źródłaLogan, 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.
Pełny tekst źródłaTodd, Adam. "The role and inhibition of reactive oxygen species (ROS) in psoriasis". Thesis, University of Sunderland, 2009. http://sure.sunderland.ac.uk/3699/.
Pełny tekst źródła