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Relevant bibliographies by topics / Oxidative inactivation

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Academic literature on the topic 'Oxidative inactivation'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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Journal articles on the topic "Oxidative inactivation"

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Gopalakrishna, R., and W. B. Anderson. "Ca2+- and phospholipid-independent activation of protein kinase C by selective oxidative modification of the regulatory domain." Proceedings of the National Academy of Sciences 86, no. 17 (1989): 6758–62. http://dx.doi.org/10.1073/pnas.86.17.6758.

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The susceptibility of purified protein kinase C to oxidative inactivation by H2O2 was found to be increased by Ca2+ either alone at a high (5 mM) concentration or at a low (approximately 50 microM) concentration along with phosphatidylserine and diacylglycerol and by tumor-promoting phorbol esters even in the absence of Ca2+. This suggested that the membrane-bound and/or catalytically active form of protein kinase C is relatively more susceptible to oxidative inactivation. Although both the regulatory and catalytic domains of protein kinase C were susceptible to oxidative inactivation, a selec

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Andersson, S., A. Kheiter, and T. A. Merritt. "Oxidative Inactivation of Surfactants." Lung 177, no. 3 (1999): 179–89. http://dx.doi.org/10.1007/pl00007639.

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Janero, D. R., and C. Yarwood. "Oxidative modulation and inactivation of rabbit cardiac adenylate deaminase." Biochemical Journal 306, no. 2 (1995): 421–27. http://dx.doi.org/10.1042/bj3060421.

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Oxidative stress and adenine nucleotide catabolism occur concomitantly in several disease states, such as cardiac ischaemia-reperfusion, and may act as synergistic determinants of tissue injury. However, the mechanisms underlying this potential interaction remain ill-defined. We examined the influence of oxidative stress on the molecular, kinetic and regulatory properties of a ubiquitous AMP-catabolizing enzyme, adenylate deaminase (AMPD) (EC 3.5.4.6). To this intent, rabbit heart AMPD and an H2O2/ascorbate/iron oxidation system were employed. Enzyme exposure to the complete oxidation system a

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Andersson, Sture, Ahmed Kheiter, Erlinda Manalo, John Amirkhanian, and T. Allen Merritt. "OXIDATIVE INACTIVATION OF SURFACTANT † 1929." Pediatric Research 39 (April 1996): 324. http://dx.doi.org/10.1203/00006450-199604001-01953.

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Ceccaldi, Pierre, Marta C. Marques, Vincent Fourmond, Inês Cardoso Pereira, and Christophe Léger. "Oxidative inactivation of NiFeSe hydrogenase." Chemical Communications 51, no. 75 (2015): 14223–26. http://dx.doi.org/10.1039/c5cc05930e.

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We propose a resolution to the paradox that spectroscopic studies of NiFeSe hydrogenase have not revealed any major signal attributable to Ni<sup>III</sup> states formed upon reaction with O<sub>2</sub>, despite the fact that two inactive states are formed upon either aerobic or anaerobic oxidation.

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Parkkinen, Jaakko, Outi Vääränen, and Elina Vahtera. "Plasma Ascorbate Protects Coagulation Factors against Photooxidation." Thrombosis and Haemostasis 75, no. 02 (1996): 292–97. http://dx.doi.org/10.1055/s-0038-1650263.

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SummaryIt has been suggested that proteins, unlike lipids, are not protected against oxidative damage by antioxidants in plasma. We have studied the effect of photodynamic virus inactivation treatment of fresh human plasma on coagulation factor activities. Photodynamic treatment generates singlet oxygen which causes inactivation of fibrinogen and factor VIII. Other coagulation factors or anticoagulant proteins are clearly less affected. We found that there is an inverse correlation between the extent of coagulation factor inactivation during the treatment and the plasma ascorbate concentration

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Cavarra, Eleonora, Monica Lucattelli, Federica Gambelli, et al. "Human SLPI inactivation after cigarette smoke exposure in a new in vivo model of pulmonary oxidative stress." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (2001): L412—L417. http://dx.doi.org/10.1152/ajplung.2001.281.2.l412.

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The role of oxidative stress in inactivating antiproteases is the object of debate. To address this question, we developed an in vivo model of pulmonary oxidative stress induced by cigarette smoke (CS) in mice. The major mouse trypsin inhibitor contrapsin is not sensitive to oxidation, and the mouse secretory leukoprotease inhibitor (SLPI) does not inhibit trypsin. Instead, human recombinant (hr) SLPI inhibits trypsin and is sensitive to oxidation. Thus we determined the effect of CS in vivo on hrSLPI antiproteolytic function in the airways of mice. CS caused a significant decrease in total an

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Kim, Sunghwan, Dionisia P. Sideris, Carolyn S. Sevier, and Chris A. Kaiser. "Balanced Ero1 activation and inactivation establishes ER redox homeostasis." Journal of Cell Biology 196, no. 6 (2012): 713–25. http://dx.doi.org/10.1083/jcb.201110090.

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The endoplasmic reticulum (ER) provides an environment optimized for oxidative protein folding through the action of Ero1p, which generates disulfide bonds, and Pdi1p, which receives disulfide bonds from Ero1p and transfers them to substrate proteins. Feedback regulation of Ero1p through reduction and oxidation of regulatory bonds within Ero1p is essential for maintaining the proper redox balance in the ER. In this paper, we show that Pdi1p is the key regulator of Ero1p activity. Reduced Pdi1p resulted in the activation of Ero1p by direct reduction of Ero1p regulatory bonds. Conversely, upon d

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CONCONI, Mariangela, Isabelle PETROPOULOS, Istvan EMOD, Evelyne TURLIN, Francis BIVILLE, and Bertrand FRIGUET. "Protection from oxidative inactivation of the 20S proteasome byheat-shock protein 90." Biochemical Journal 333, no. 2 (1998): 407–15. http://dx.doi.org/10.1042/bj3330407.

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Heat-shock protein 90 (Hsp 90) has been implicated in both protection against oxidative inactivation and inhibition of the multicatalytic proteinase (MCP, also known as 20 S proteasome). We report here that the protective and inhibitory effects of Hsp 90 depend on the activation state of the proteasome. Hsp 90 (and also α-crystallin) inhibits the N-Cbz-Leu-Leu-Leu-MCA-hydrolysing activity (Cbz = benzyloxycarbonyl; MCA = 7-amido-4-methylcoumarin) when the rat liver MCP is in its latent form, but no inhibitory effects are observed when the MCP is in its active form. Metal-catalysed oxidation of

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Marcillat, O., Y. Zhang, and K. J. A. Davies. "Oxidative and non-oxidative mechanisms in the inactivation of cardiac mitochondrial electron transport chain components by doxorubicin." Biochemical Journal 259, no. 1 (1989): 181–89. http://dx.doi.org/10.1042/bj2590181.

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The quinonoid anthracycline, doxorubicin (Adriamycin) is a potent anti-neoplastic agent whose clinical use is limited by severe cardiotoxicity. Mitochondrial damage is a major component of this cardiotoxicity, and rival oxidative and non-oxidative mechanisms for inactivation of the electron transport chain have been proposed. Using bovine heart submitochondrial preparations (SMP) we have now found that both oxidative and non-oxidative mechanisms occur in vitro, depending solely on the concentration of doxorubicin employed. Redox cycling of doxorubicin by Complex I of the respiratory chain (whi

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Dissertations / Theses on the topic "Oxidative inactivation"

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Goudie, Alison C. "Microbial inactivation potential of electrically-generated oxidative technologies." Thesis, University of Strathclyde, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428885.

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Lubbe, Lizelle. "Investigating domain-selective angiotensin converting enzyme inhibition and oxidative inactivation." Doctoral thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29324.

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Angiotensin converting enzyme (ACE) is a zinc metalloprotease comprised of two highly homologous, catalytically active domains (90% active site identity and 60% sequence similarity). The C-domain is responsible for blood pressure regulation via angiotensin I cleavage while the N-domain inactivates an antifibrotic peptide Acetyl-Ser-Asp-Lys-Pro (AcSDKP). Since selective N-domain inhibition will result in AcSDKP accumulation, it shows promise for the treatment of fibrosis without affecting blood pressure. Low bioavailability, however, precludes the use of currently available N-selective ACE inhi

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Barber, Drew. "Selenium In Thioredoxin Reductase: Resistance To Oxidative Inactivation, Oxidation States, And Reversibility Of Chemical Reactions." ScholarWorks @ UVM, 2018. https://scholarworks.uvm.edu/graddis/943.

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Selenium is a required trace element which was originally discovered by the Swedish chemist Jons Jacob Berzelius in 1817. It was initially believed to be a toxin as it was identified as being the cause of hoof maladies and excessive hair loss in horses that feed upon plants with high selenium content. It wasn’t until 1957 that the potential contributions of selenium to physiology were first demonstrated. Selenium is now known to play a critical role in the maintenance of human health. Interestingly, unlike other trace metals/semi-metals, selenium is directly incorporated into proteins in the f

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Boylston, Jennifer A. "FHIT inactivation combined with cigarette smoke enhances the oxidative stress response." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/1295.

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The FHIT gene is located on the most fragile site in the human genome. FHIT gene deletions are among the earliest and most frequent events in carcinogenesis, particularly in carcinogen-exposed tissue. Previous work in mouse and cell culture models established FHIT to be an authentic tumor suppressor. Re-expression of FHIT in cell culture causes cell death via initiation of apoptosis, but the precise mechanism underlying this process is unclear. It is well established that cellular transition from normal to transformed occurs in multiple steps and requires the accumulation of several genetic ch

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Goto, Toshihiko. "Liver specific Prox1 inactivation causes hepatic injury and glucose intolerance in mice." Kyoto University, 2017. http://hdl.handle.net/2433/225976.

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Alves, Eliana Sousa Cruz Ferreira. "Photodynamic inactivation of bacteria by cationic porphyrins : their cellular targets and potential environmental applications." Doctoral thesis, Universidade de Aveiro, 2013. http://hdl.handle.net/10773/12435.

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Doutoramento em Biologia<br>Photodynamic inactivation (PDI) is defined as the process of cell destruction by oxidative stress resulting from the interaction between light and a photosensitizer (PS), in the presence of molecular oxygen. PDI of bacteria has been extensively studied in recent years, proving to be a promising alternative to conventional antimicrobial agents for the treatment of superficial and localized infections. Moreover, the applicability of PDI goes far beyond the clinical field, as its potential use in water disinfection, using PS immobilized on solid supports, is cur

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El, bakkali taheri Nadia. "Oxydase de l'acide 1-aminocyclopropane carboxylique : mode d'action et inactivation." Thesis, Aix-Marseille 3, 2011. http://www.theses.fr/2011AIX30042.

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L’oxydase de l’acide 1-AminoCyclopropane Carboxylique (ACC Oxydase, ACCO) catalyse la formation de l’éthylène, hormone essentielle à la vie des plantes. L’ACCO catalyse l’oxydation de l’ACC en éthylène en présence de dioxygène et de deux électrons (fournis in vitro par l’ascorbate). L'activité de l'enzyme requière également, pour des raisons encore incomprises, la présence de CO2 sous la forme d'ions bicarbonates. Il s’agit d’une enzyme qui contient un ion fer(II) dans un environnement non-hémique au site actif. Etant donné l’importance de l’éthylène chez les plantes, l’ACCO, ainsi que les aut

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Buehlmann, Peter Hamilton. "Balancing Bromate Formation, Organics Oxidation, and Pathogen Inactivation: The Impact of Bromate Suppression Techniques on Ozonation System Performance in Reuse Waters." Thesis, Virginia Tech, 2019. http://hdl.handle.net/10919/93530.

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Ozonation is an integral process in ozone-biofiltration treatment systems and is beginning to be widely adopted worldwide for water reuse applications. Ozone is effective for pathogenic inactivation and organics oxidation: both increasing assimilable organic carbon for biofiltration and eliminating trace organic contaminants which may pose a threat to human health. However, ozone can also form disinfection byproducts such as bromate from the oxidation of naturally occurring anion bromide. Bromate is a known human carcinogen and is regulated by the EU, WHO, and USEPA to a maximum limit of 10µg/

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Machado, Luciana E. S. F., Tun-Li Shen, Rebecca Page, and Wolfgang Peti. "The KIM-family protein-tyrosine phosphatases use distinct reversible oxidation intermediates: Intramolecular or intermolecular disulfide bond formation." AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2017. http://hdl.handle.net/10150/624478.

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The kinase interaction motif (KIM) family of protein-tyrosine phosphatases (PTPs) includes hematopoietic protein-tyrosine phosphatase (HePTP), striatal-enriched protein-tyrosine phosphatase (STEP), and protein-tyrosine phosphatase receptor type R (PTPRR). KIM-PTPs bind and dephosphorylate mitogen-activated protein kinases (MAPKs) and thereby critically modulate cell proliferation and differentiation. PTP activity can readily be diminished by reactive oxygen species (ROS), e.g. H2O2, which oxidize the catalytically indispensable active-site cysteine. This initial oxidation generates an unstable

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Garton, Mary Joanne. "Photocatalytic oxidation of selected organic contaminants and inactivation of microorganisms in a continuous flow reactor packed with titania-doped silica." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010842.

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Books on the topic "Oxidative inactivation"

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Ramakrishnan, Venugopal. Oxidative inactivation of glucose oxidase. National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Book chapters on the topic "Oxidative inactivation"

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Valdez, Laura B., Silvina S. Bombicino, Darío E. Iglesias, Ivana A. Rukavina-Mikusic, and Verónica D’Annunzio. "Mitochondrial Complex I Inactivation After Ischemia-Reperfusion in the Stunned Heart." In Biochemistry of Oxidative Stress. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45865-6_16.

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Reilly, Christopher A. "Cytochrome P450-Dependent Modification of Capsaicinoids: Pharmacological Inactivation and Bioactivation Mechanisms." In Role of Capsaicin in Oxidative Stress and Cancer. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6317-3_6.

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Vissers, Margret C. M., and Christine C. Winterbourn. "Oxidative Inactivation of Neutrophil Granule Proteinases: Implications for Neutrophil-Mediated Proteolysis." In Oxygen Radicals in Biology and Medicine. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5568-7_136.

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Subelzu, N., S. Bartesaghi, A. de Bem, and R. Radi. "Oxidative Inactivation of Nitric Oxide and Peroxynitrite Formation in the Vasculature." In ACS Symposium Series. American Chemical Society, 2015. http://dx.doi.org/10.1021/bk-2015-1200.ch004.

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Jouanneau, Y. "Oxidative Inactivation of Ring-Cleavage Extradiol Dioxygenases: Mechanism and Ferredoxin-Mediated Reactivation." In Handbook of Hydrocarbon and Lipid Microbiology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-77587-4_75.

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Sun, Hongwei, Guiying Li, and Taicheng An. "Bacterial Oxidative Stress Responses and Cellular Damage Caused by Photocatalytic and Photoelectrocatalytic Inactivation." In Green Chemistry and Sustainable Technology. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-53496-0_12.

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Robey, M., S. F. Park, and B. M. Mackey. "Role of Oxidative Stress in the Inactivation of Escherichia coli by High Hydrostatic Pressure." In Advances in High Pressure Bioscience and Biotechnology. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60196-5_20.

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Nasser, Abidelfatah M. "Inactivation of Cryptosporidium by Advanced Oxidation Processes." In The Handbook of Environmental Chemistry. Springer International Publishing, 2017. http://dx.doi.org/10.1007/698_2017_85.

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Guerra-Rodriguez, Sonia, Jorge Rodríguez-Chueca, José A. Peres, and Marco S. Lucas. "Chapter 9. Inactivation of Pathogenic Microorganisms with Sulfate Radical-based Advanced Oxidation Processes." In Persulfate-based Oxidation Processes in Environmental Remediation. Royal Society of Chemistry, 2022. http://dx.doi.org/10.1039/9781839166334-00229.

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Cchjda, Koh. "ROS damage to protein." In Experimental protocols for reactive oxygen and nitrogen species. Oxford University PressOxford, 2000. http://dx.doi.org/10.1093/oso/9780198506683.003.0074.

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Abstract Several lines of evidence indicate that protein oxidation by free radicals and the subsequent accumulation of oxidatively modified proteins, which could be an early indication of oxygen radical-mediated tissue damage, have been found in cells during ageing, after oxidative stress, and in various pathological states including premature ageing diseases, muscular dystrophy, rheumatoid arthritis, and atherosclerosis (1). Furthermore, free radical-mediated oxidative inactivation of enzymes, especially by metal-catalysed oxidation systems, have been postulated as marking steps in enzyme tur

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Conference papers on the topic "Oxidative inactivation"

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Remels, Alexander, Koen Verhees, Harry Gosker, Annemie Schols, Ramon Langen та Alexander Remels. "Inactivation of glycogen synthase kinase 3β (GSK-3β) enhances skeletal muscle oxidative metabolism". У Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1226.

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Ngkelo, Anta, John A. Marwick, Laurie Stevens, Paul Kirkham, and Ian M. Adcock. "Oxidative Stress Induced Inactivation Of The Glycogen Synthase Kinase 3beta Reduces Steroid Function In Human Monocytes." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2802.

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Li, G., S. S. Nair, S. J. Lees, and F. W. Booth. "Regulation of G2/M Transition in Mammalian Cells by Oxidative Stress." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-82349.

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The regulation of the G2/M transition for the mammalian cell cycle has been modeled using 19 states to investigate the G2 checkpoint dynamics in response to oxidative stress. A detailed network model of G2/M regulation is presented and then a “core” subsystem is extracted from the full network. An existing model of Mitosis control is extended by adding two important pathways regulating G2/M transition in response to DNA damage induced by oxidative stress. Model predictions indicate that the p53 dependent pathway is not required for initial G2 arrest as the Chk1/Cdc25C pathway can arrest the ce

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Kim, H., C. Kim, J. Kang, S. Lee, and J. Yoon. "ECG Suppresses Oxidative Stress-Induced MUC5AC Overexpression in Human Primary Airway Epithelial Cells through the Inactivation of Epidermal Growth Factor Receptor." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6302.

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Rabbani, Naila, Paul John Thornalley, Maryam Al-Motawa, and Mingzhan Xue. "Vulnerabilities of the SARS-Cov-2 Virus to Proteotoxicity – Opportunity for Repurposed Chemotherapy of COVID-19 Infection." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0291.

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The global pandemic of COVID-19 disease caused by infection with the SARS-CoV-2 Coronavirus, has produced an urgent requirement and search for improved treatments whilst effective vaccines are developed. A strategy for improved drug therapy is to increase levels of endogenous reactive metabolites for selective toxicity to SARS-CoV-2 by preferential damage to the viral proteome. Key reactive metabolites producing major quantitative damage to the proteome in physiological systems are: Reactive oxygen species (ROS) and the reactive glycating agent methylglyoxal (MG); cysteine residues and arginin

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Gomes, Ana, Ana Sampaio, Sara Silva, José R. Fernandes, José A. Peres, and Marco S. Lucas. "Inactivation of Candida albicans in Water Using Advanced Oxidation Processes." In ASEC 2023. MDPI, 2023. http://dx.doi.org/10.3390/asec2023-15302.

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Jinlong, Zuo. "Inactivation of Cyclops by Chemical Oxidation in a Drinking Water Plant." In 2009 International Conference on Environmental Science and Information Application Technology, ESIAT. IEEE, 2009. http://dx.doi.org/10.1109/esiat.2009.556.

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Luster-Teasley, Stephanie, Christopher Jackson, and Chanel Rogers. "Inactivation of Pathogens in Agricultural Wastewater Using Controlled Release Chemical Oxidation Polymer System." In World Environmental and Water Resources Congress 2011. American Society of Civil Engineers, 2011. http://dx.doi.org/10.1061/41173(414)163.

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Reszka, KJ, DW McGraw та BE Britigan. "Airway Peroxidases Can Catalyze Inactivating Oxidation/Nitration of β-Agonists." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3643.

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Niwa, A., and K. Hamashima. "Effect of M-CrAlY Coating for Corrosion Resistance in Specific High Temperature Atmosphere." In ITSC2010, edited by B. R. Marple, A. Agarwal, M. M. Hyland, et al. DVS Media GmbH, 2010. http://dx.doi.org/10.31399/asm.cp.itsc2010p0298.

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Abstract In the glass manufacturing, stainless-steel parts are used in characteristic corrosive reduction atmosphere at high temperature. The reactive products, that are induced by volatilization from the stainless steel surface, cause defects of the glass in this usage. Some thermal spraying coating of thermal-resistant alloys is tested in this study for the protection to the volatilization. It is clarified that, the Ni-Cr-Al-Y film, containing plate-like metal oxide dispersions, shows an outstanding effect as followings; 1) The diffusion rate of Fe from a stainless substrate in this coating

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Reports on the topic "Oxidative inactivation"

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Dickman, Martin B., and Oded Yarden. Modulation of the Redox Climate and Phosphatase Signaling in a Necrotroph: an Axis for Inter- and Intra-cellular Communication that Regulates Development and Pathogenicity. United States Department of Agriculture, 2011. http://dx.doi.org/10.32747/2011.7697112.bard.

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The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotiorum. The focus in this project is on the elucidation of the signaling events and environmental cues that contribute to broad pathogenic success of S. sclerotiorum. In this proposal, we have taken advantage of the recent conceptual (ROS/PPs signaling) and technical (genome sequence availability and gene inactivation possibilities) developments to address the following questions, as appear in our research goals stated below, specifically concerning the involvement of RE

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Ohad, Itzhak, and Himadri Pakrasi. Role of Cytochrome B559 in Photoinhibition. United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7613031.bard.

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The aim of this research project was to obtain information on the role of the cytochrome b559 in the function of Photosystem-II (PSII) with special emphasis on the light induced photo inactivation of PSII and turnover of the photochemical reaction center II protein subunit RCII-D1. The major goals of this project were: 1) Isolation and sequencing of the Chlamydomonas chloroplast psbE and psbF genes encoding the cytochrome b559 a and b subunits respectively; 2) Generation of site directed mutants and testing the effect of such mutation on the function of PSII under various light conditions; 3)

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