Bibliografie tematiche / Reactive oxygen species

Letteratura scientifica selezionata sul tema "Reactive oxygen species"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 27 luglio 2024

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Articoli di riviste sul tema "Reactive oxygen species"

1

Drobot, L. B. "Reactive oxygen species in signal transduction". Ukrainian Biochemical Journal 85, n. 6 (27 dicembre 2013): 207–17. http://dx.doi.org/10.15407/ubj85.06.209.

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Kumar, Vishnu, e Abdus Salam. "A REVIEW ON REACTIVE OXYGEN AND NITROGEN SPECIES". ERA'S JOURNAL OF MEDICAL RESEARCH 5, n. 1 (giugno 2018): 59–66. http://dx.doi.org/10.24041/ejmr2018.63.

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Jadko, S. I. "Histone deacetylase activity and reactive oxygen species content". Ukrainian Biochemical Journal 87, n. 3 (27 giugno 2015): 57–62. http://dx.doi.org/10.15407/ubj87.03.057.

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Bayr, Hülya. "Reactive oxygen species". Critical Care Medicine 33, Suppl (dicembre 2005): S498—S501. http://dx.doi.org/10.1097/01.ccm.0000186787.64500.12.

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Morrell, Craig N. "Reactive Oxygen Species". Circulation Research 103, n. 6 (12 settembre 2008): 571–72. http://dx.doi.org/10.1161/circresaha.108.184325.

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Bukoski, Richard D. "Reactive oxygen species". Journal of Hypertension 20, n. 11 (novembre 2002): 2141–43. http://dx.doi.org/10.1097/00004872-200211000-00009.

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Krötz, Florian, Hae-Young Sohn e Ulrich Pohl. "Reactive Oxygen Species". Arteriosclerosis, Thrombosis, and Vascular Biology 24, n. 11 (novembre 2004): 1988–96. http://dx.doi.org/10.1161/01.atv.0000145574.90840.7d.

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SURI, R. K., M. S. RATNA, V. DHAWAN, A. GUPTA, R. GUPTA, K. SHARMA, S. K. S. THINGNAM, G. D. PURI, S. MADHULIKA e N. K. GANGULY. "Reactive Oxygen Species." Annals of the New York Academy of Sciences 793, n. 1 Myocardial Pr (settembre 1996): 366–70. http://dx.doi.org/10.1111/j.1749-6632.1996.tb33528.x.

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N. Agbedanu, Prince, Troy B. Puga, Joshua Schafer, Pearce Harris, Gary Branum e Nora Strasser. "Investigation of Reactive Oxygen Species production in Human Hepatocytes". Gastroenterology Pancreatology and Hepatobilary Disorders 6, n. 2 (12 gennaio 2022): 01–06. http://dx.doi.org/10.31579/2641-5194/058.

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Abstract (sommario):
1. Aim/Background: Reactive oxygen species (ROS) have been identified as compounds responsible for producing cellular damage. The purpose of this research is to examine if there is production of reactive oxygen species through free radical intermediates within human hepatocytes treated with morphine, bilirubin, or furosemide. The investigation examines the early stages of biotransformation by measuring the levels of reactive oxygen species produced inside of the treated hepatocytes within the first and second hours of treatment. The experiment was designed upon a case of a jaundiced (elevated bilirubin) infant who received morphine and furosemide and later died through unknown mechanisms. The experiment looks to examine if these drug compounds could contribute to cellular damage. This can help to further understand the potential interactions and complications of free radical intermediates produced during the phases of biotransformation. 2. Method: Previously cultured human hepatocytes were washed by centrifugation and re-suspended in 1x supplemental buffer to a concentration of 1x106 cells/mL and seeded in a dark clear bottom 96-well microplate at 100,000 stained cells/well. The cells were treated with either furosemide, morphine, bilirubin, a Tert-Butyl hydro peroxide (TBHP) positive control, or left as a background. Reactive oxygen generated in the presence of these agents were quantified by fluorescence excitation/emission measurement at 495nm/529nm. Fluorescence was measured at one and two hours. ROS generated convert 2',7'-dichlorodihydrofluorescein diacetate to 2',7'-dichlorodihydrofluorescein within the cells, which fluoresces. The fluorescence intensity detected is equivalent to the level of ROS generated. Wells that were untreated were used as blanks and subtracted from background and TBPH. 3. Results: Furosemide and Morphine did not produce statistically significant levels of ROS (p >0.05) above the background in both hours 1 and 2 of biotransformation and ROS measurement (Figure 1). Although Bilirubin did not produce statistically significant (p >0.05) levels of ROS above the background (Figure 2) during the first hour, it did produce statistically significant levels in the second hour of biotransformation. Each compound’s level of ROS was reduced during the second hour, signaling the removal of intermediate ROS metabolites (Figure 2). The production of ROS in each compound signifies that there is biotransformation to an intermediate that produces ROS. 4. Conclusion: The production of ROS above the background by each of the compounds shows there is an intermediate free radical compound that is produced during the biotransformation of each compound [21]. In this study, although furosemide and morphine did not produce statistically significant levels of ROS in both hours of biotransformation, bilirubin did produce significant levels of ROS in the second hour of biotransformation. This finding is in line with previous studies that shows morphine to offer protective effects against ROS production [16, 17]; and bilirubin demonstrating deleterious production of ROS at high doses [18]. Further work must be done to examine the correlation between the levels of ROS and extent of hepatocellular damage.
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TANAKA, Katsuya, e David C. WARLTIER. "Mechanism of Anesthetic Preconditioning: A Role for Reactive Oxygen Species". JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 25, n. 2 (2005): 206–12. http://dx.doi.org/10.2199/jjsca.25.206.

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Tesi sul tema "Reactive oxygen species"

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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.

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Stanczak, Anna. "Reactive oxygen species in laundry applications". Thesis, Durham University, 2018. http://etheses.dur.ac.uk/12885/.

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Chapter 1 is divided into two parts, the first gives a brief review of oxygen-based bleaching agents commonly used in powder laundry detergent with emphasis on the properties of hydrogen peroxide and peroxy acids. In the second part of the literature review, different methods of detection of Reactive Oxygen Species (ROS) are discussed. Chapter 2 discusses analytical techniques used throughout this thesis, mainly focusing on the fluorescence and UV-Vis spectroscopy, as well as imaging techniques: Image Analysis and Diffuse Reflectance Spectroscopy. This chapter provides also detailed experimental procedures. Chapter 3 includes the results and discussion part of the thesis. The process of the development of fluorescent probes for the most relevant ROS in laundry applications: hydrogen peroxide, peroxy acid, hydroxyl radicals and singlet oxygen is discussed. The established toolbox of molecular probes consists of: terephthalic acid, 9,10-anthracenediyl-bis(methylene)dimalonic acid and 2-naphthylboronic acid for detection of hydroxyl radicals, singlet oxygen and peroxides, respectively. Chapter 4 reports the kinetic parameters of the ROS generated from genuine bleach source in simplified model system (alkaline solution) established with the developed toolbox of molecular probes. Chapter 5 introduces four model dyes which represent genuine stains: curcumin, crocin, betanin and chlorophyllin. The impact of pH on the bleaching of the model dyes was investigated as well as bleaching kinetic parameters. The behaviour of peroxy acids generated from bleach sources in the presence of model dyes was determined with the toolbox of molecular probes developed in Chapter 3. Chapter 6 examines the bleaching performance of different ROS on genuine stains deposed on fabric: grass, tomato, curry, red wine and tea with Image Analysis technique and Diffuse Reflectance Spectroscopy. In the second part of the chapter the behaviour of the bleaching agents in the presence of stains was investigated.
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Wu, Wan Man. "Reactive oxygen species and murine malaria". Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26446.

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The aim of this study was to investigate the role of ROS in the protective and pathological immune response during malarial infection. For this purpose, four isolates of Plasmodium parasites (P. berghei ANKA, P. vinckei, P. berghei K152 and P. chabaudi) and two different inbred strains of mice (CBA and DBA) were used. The patterns of mortality varied between the different mouseparasite strain combinatio ns. The mortality of CBA mice infected with P. vinckei and P. berghei K152, and DBA mice infected with P. berghei ANKA, related to the levels of parasitaemia. However early mortality of CBA mice infected with P. berghei ANKA did not relate to the parasitaem ia level but to the onset of neurologica l symptoms. Over 90% of P. chabaudi—infected CBA mice recovered from the infection. The morphologi cal examinatio n of brain tissues obtained from P. berghei ANKA-infec ted CBA mice on day 7 post-inocul ation showed haemorrag e, oedema and the infiltration of mononucle ar cells. Measurement of the permeability of the blood-brain barrier by injection of Evans blue showed the dye leaking into the brain parenchyma, suggesting a dysfunction of the barrier in this mouse model. The hypothesis that ROS play a role in the anti—malaria response was supported by previous studies demonstrati ng that malaria parasites are killed by ROS in vivo and in vitro (reviewed in Hunt & Stocker. 1990). To further test the hypothesis. the oxidative burst ability of splenic macrophage s and peripheral monocytes taken from different mouse-para site strain combinations was examined. There was a significant increase of superoxide production by splenic macrophag es at the early stage of all the infections and the spleen weight gradually increased during all the infections. Furthermore, the oxidative burst ability of monocytes was significantly increased in the late stage of all the infections, which was accompanied by increased peripheral WBC numbers, especially in the numbers of monocytes and PMNs in all the infections except the P. berghei ANKA infection in CBA mice. Of the four strains of parasites infecting CBA mice, the self-resol ving P. Chabaudi infection induced the greatest PMA-stimulable response superoxide anion production on certain days after parasite in inoculation in both splenic macrophages and monocytes . Conversely, the P. vinckei infection induced the lowest response, which may partly explain why the parasites generated faster in these mice than in the other three strains. Malaria parasites are able to induce immunosup pression at the early stage of infection as shown by the decline in the total number of WBC and the decrease of superoxide production by monocytes. This immunosuppresion may help explain why the parasites can survive even when their numbers are. small. TNF and IFN—y are known as major mediatory factors involved in the development of cerebral malaria. This was supported by the cytokine gene expression studies which showed that both TNF and IFN-y mRNAs were expressed in the brains of mice with cerebral malaria. These cytokines may stimulate mononuclear phagocytes to produce other soluble factors to cause cerebral damage. ROS release d from mononuclear phagocytes are thought to be crucial factors involved in the development of cerebral malaria (Hunt et al., 1991). However , the oxidative burst ability of splenic macrophages and monocytes in the P. berghei—ANKA infected CBA mice, which suffered cerebral malaria and died early in the infection, was lower than that in the same infection in DBA mice which recovered from the cerebral lesion but died at a later stage of infection with a high level of parasitaemia. Further more, lipid peroxidation studies showed that there was no significant difference in brain MDA formation between control mice and the mice with cerebral malaria . These results fail to provide evidence for a role of ROS in the development of cerebral malaria . Further studies to investigate lipid peroxidation and redox. status of the brain in cerebral malaria using HPLC are required.
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Yu, Tian-Wei. "Genotoxic damage induced by reactive oxygen species". Thesis, University of Surrey, 1997. http://epubs.surrey.ac.uk/764/.

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Baumber, 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.

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Xie, Ruiyu. "Reactive Oxygen Species-Induced Necrotic Cell Death". Diss., The University of Arizona, 2009. http://hdl.handle.net/10150/195215.

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Mechanisms of cell death extend beyond the simple apoptosis/necrosis relationship to include regulated modes of cell death that do not readily fit either of the classic descriptors. One such mechanism of cell death involves poly(ADP-ribose)polymerase-1 (PARP-1)-mediated cell death. 2,3,5-Tris(Glutathion-S-yl)-hydroquinone (TGHQ), a reactive oxygen species (ROS) generating nephrotoxic and nephrocarcinogenic metabolite of hydroquinone, causes necrotic renal cell death, the basis for which is unclear. We therefore investigated TGHQ-mediated cell death in human renal proximal tubule epithelial HK-2 cells. TGHQ induced ROS generation, DNA strand breaks, hyperactivation of PARP-1, rapid depletion of nicotinamide adenine dinucleotide (NAD), elevations in intracellular Ca2+ concentrations, loss of mitochondrial membrane potential, and subsequent necrotic cell death. Interestingly, PARP-1 hyperactivation was not accompanied by the translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus, a process usually associated with PARP-dependent cell death. Inhibition of PARP-1 with PJ34 blocked TGHQ-mediated accumulation of poly(ADP-ribose) polymers, NAD consumption, and the consequent necrotic cell death. However, HK-2 cell death was only delayed by PJ34, and cell death remained necrotic in nature. In contrast, chelation of intracellular Ca2+ with BAPTA-AM completely abrogated TGHQ-induced necrotic cell death. Ca2+ chelation not only prevented the collapse in the mitochondrial potential but also attenuated PARP-1 hyperactivation. Conversely, inhibition of PARP-1 modulated TGHQ-mediated changes in Ca2+ homeostasis. Moreover, TGHQ caused a sequential oxidation of peroxiredoxin III (PrxIII), a protein considered the primary antioxidant defense within mitochondria. Thus, TGHQ induced two acidic shifts in PrxIII, with both pI shifted spots representing oxidized forms of PrxIII. Transient expression of a dominant negative version of PrxIII resulted in a significant increase in TGHQ-induced cytotoxicity, whereas overexpression of wild-type PrxIII significantly attenuated cytotoxicity. Our studies provide new insights into PARP-1-mediated necrotic cell death. Changes in intracellular Ca2+ concentrations appear to couple PARP-1-hyperactivation to subsequent cell death, but in the absence of AIF release from mitochondria. NAD depletion, mitochondrial membrane depolarization, Ca2+-mediated calpain activation, and PrxIII oxidation, all contribute to TGHQ-driven ROS-mediated necrotic cell death.
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Cowgill, Danielle Lee. "FIELD DECTION DEVICE OF REACTIVE OXYGEN SPECIES". DigitalCommons@CalPoly, 2013. https://digitalcommons.calpoly.edu/theses/1107.

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Traumatic brain injuries (TBIs) contribute to approximately 30.5% of all injury related deaths in the United States per year and approximately 1.7 million TBIs per year occur as an isolated injury or other injury. Military personnel are exposed to TBIs and have less availability to resources traditionally used to diagnose a TBI. Reactive oxygen species (ROS) play a large role in secondary traumatic brain damage, especially lipid peroxidation, following TBIs. One of the principle and most studied byproducts of lipid peroxidation is malondialdehyde (MDA). The focus of this paper was to create an initial proof-of-concept field diagnostic device to detect ROS, or constituents, following a TBI. The device was divided into three main sections: blood separation, sample separation, and detection. This thesis report examined the blood and sample separation sections of the device; however the blood separation was not developed due to university restrictions. Pre-fabricated microfluidic chips and a confocal microscope were used for the separation. Pressure was first used to drive the fluid through the channel to observe functionality of the chip with 10 um microspheres and then a MDA solution once the spheres were successful. When fluid successfully flowed through the channels with pressure, voltage was then applied to the channels to create a capillary electrophoresis (CE) system. The CE system was tested with the spheres first and then the MDA solution upon successful demonstration of voltage-driven flow. Analysis of the images was performed using ImageJ software in attempt to determine the velocity of the spheres and MDA. The results of the system appeared to successfully drive the MDA with voltage-driven flow after waiting for the residual effects of the applied pressure to reduce. However, any conclusions require more experimental data.
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Yamamoto, 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.

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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 physiological ROS levels trigger the protective pathways, while p53 behaves more like a cell killer under cytotoxic oxidative stress.
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Lloyd, 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.

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Libri sul tema "Reactive oxygen species"

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Schmitt, Franz-Josef, e Suleyman I. Allakhverdiev, a cura di. Reactive Oxygen Species. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119184973.

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Espada, Jesús, a cura di. Reactive Oxygen Species. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0896-8.

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Schmidt, Harald H. H. W., Pietro Ghezzi e Antonio Cuadrado, a cura di. Reactive Oxygen Species. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68510-2.

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Faizan, Mohammad, Shamsul Hayat e S. Maqbool Ahmed, a cura di. Reactive Oxygen Species. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5.

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Mhamdi, Amna, a cura di. Reactive Oxygen Species in Plants. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2469-2.

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Singh, Vijay Pratap, Samiksha Singh, Durgesh Kumar Tripathi, Sheo Mohan Prasad e Devendra Kumar Chauhan, a cura di. Reactive Oxygen Species in Plants. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119324928.

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Sachdev, Swati, Shamim Akhtar Ansari e Mohammad Israil Ansari. Reactive Oxygen Species in Plants. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9884-3.

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Rio, Luis Alfonso, e Alain Puppo, a cura di. Reactive Oxygen Species in Plant Signaling. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00390-5.

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Bhattacharjee, Soumen. Reactive Oxygen Species in Plant Biology. New Delhi: Springer India, 2019. http://dx.doi.org/10.1007/978-81-322-3941-3.

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Gilbert, Daniel L., e Carol A. Colton. Reactive Oxygen Species in Biological Systems. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/b113066.

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Capitoli di libri sul tema "Reactive oxygen species"

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Ali, Mohd Soban, Asif Hussain Hajam, Mohammad Suhel, Sheo Mohan Prasad e Gausiya Bashri. "The Dual Role of Reactive Oxygen Species as Signals that Influence Plant Stress Tolerance and Programmed Cell Death". In Reactive Oxygen Species, 161–77. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_10.

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Shehzad, Junaid, e Ghazala Mustafa. "Mechanism of Reactive Oxygen Species Regulation in Plants". In Reactive Oxygen Species, 17–41. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_2.

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Hussain, Anjuman, Chen Chen, Fangyuan Yu, S. Maqbool Ahmed e Mohammad Faizan. "Functions of Reactive Oxygen Species in Improving Agriculture and Future Crop Safety". In Reactive Oxygen Species, 53–68. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_4.

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Arif, Yamshi, Anayat Rasool Mir e Shamsul Hayat. "Reactive Oxygen Species: Role in Senescence and Signal Transduction". In Reactive Oxygen Species, 115–33. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_7.

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Somal, Manpreet Kaur, Rohan Samir Kumar Sachan, Divya Bhagat, Khusbhoo, Ritu Bala e Mukesh Kumar. "An Update on Reactive Oxygen Species Synthesis and Its Potential Application". In Reactive Oxygen Species, 1–15. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_1.

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Akeel, Arshiya, e Hassan Jaleel. "Biomolecules Targeted by Reactive Oxygen Species". In Reactive Oxygen Species, 43–51. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_3.

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Devi, Priyanka, Shipa Rani Dey, Lalit Saini, Prasann Kumar, Sonam Panigrahi e Padmanabh Dwivedi. "Toward Sustainable Agriculture: Strategies Involving Phytoprotectants Against Reactive Oxygen Species". In Reactive Oxygen Species, 229–47. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_13.

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Arshad, Huma, e Ghazala Mustafa. "Hormonal Response in Plants Influenced by Reactive Oxygen Species". In Reactive Oxygen Species, 147–60. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_9.

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Mohiuddin, Muhammad, Sidra tul Muntha, Abid Ali, Mohammad Faizan e Samrana Samrana. "The Ecology of Reactive Oxygen Species Signalling". In Reactive Oxygen Species, 69–93. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_5.

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Jahan, Ajmat, M. Masroor A. Khan, Bilal Ahmad, Khan Bilal Mukhtar Ahmed, Ram Prakash Pandey e Mohd Gulfishan. "Hydrogen Peroxide: Regulator of Plant Development and Abiotic Stress Response". In Reactive Oxygen Species, 213–28. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9794-5_12.

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Atti di convegni sul tema "Reactive oxygen species"

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Lubart, Rachel, Harry Friedman, Nili Grossman, Natalie Cohen e Haim Breitbart. "Reactive oxygen species and photobiostimulation". In BiOS Europe '97, a cura di Tiina I. Karu e Anthony R. Young. SPIE, 1997. http://dx.doi.org/10.1117/12.297993.

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Liu, Timon Cheng-Yi, Yong-Qing Wang, Xiao-Yang Xu, Xiu-Feng Zhao e Shao-Juan Hu. "Reactive Oxygen Species Mediated Generalized Photobiomodulation". In 2007 IEEE/ICME International Conference on Complex Medical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/iccme.2007.4381918.

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Suyono, Handi, e Guritno Suryokusumo. "Hyperbaric Oxygen (HBO) Heals Cell Through Reactive Oxygen Species (ROS)". In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007334001230127.

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Sun, Guo-Quan, Jue Wang, Qing Li, Ling-Bo Qian, Zhi-Guo Ye e Qiang Xia. "Acetylcholine Exerts Cardioprotection by Reducing Reactive Oxygen Species". In 2010 International Conference on Biomedical Engineering and Computer Science (ICBECS). IEEE, 2010. http://dx.doi.org/10.1109/icbecs.2010.5462443.

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Tan, Zou, Jinde Zhang, Lisheng Lin e Buhong Li. "Quantification of reactive oxygen species for photodynamic therapy". In SPIE/COS Photonics Asia, a cura di Qingming Luo, Xingde Li, Ying Gu e Yuguo Tang. SPIE, 2016. http://dx.doi.org/10.1117/12.2246526.

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Chen, Xiaoyuan. "Reactive oxygen species goes beyond photodynamic therapy (Conference Presentation)". In 17th International Photodynamic Association World Congress, a cura di Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2525919.

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Sousa, Joao Santos, Gerard Bauville, Bernard Lacour, Vincent Puech, Michel Touzeau e Jean-Luc Ravanat. "Microplasma generation of reactive oxygen species for biological applications". In 2010 IEEE 37th International Conference on Plasma Sciences (ICOPS). IEEE, 2010. http://dx.doi.org/10.1109/plasma.2010.5534048.

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Waliszewski, Przemyslaw, e Ryszard Skwarek. "Deterministic Chaos and Mitochondrial Synthesis of Reactive Oxygen Species". In 2017 21st International Conference on Control Systems and Computer Science (CSCS). IEEE, 2017. http://dx.doi.org/10.1109/cscs.2017.55.

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Price, Michael, Nakaiya Okan-Mensah, Ann Marie Santiago e David Kessel. "The role of reactive oxygen species in PDT efficacy". In SPIE BiOS: Biomedical Optics, a cura di David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.810231.

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Myers, DP, e LS Terada. "Visualization of Reactive Oxygen Species Production at Focal Adhesions." 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.a4166.

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Rapporti di organizzazioni sul tema "Reactive oxygen species"

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Lau, Yun-Fai C. Mitochondrial Structure and Reactive Oxygen Species in Mammary Oncogenesis. Fort Belvoir, VA: Defense Technical Information Center, aprile 2005. http://dx.doi.org/10.21236/ada436893.

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Lau, Yun-Fai C. Mitochondrial Structure and Reactive Oxygen Species in Mammary Oncogenesis. Fort Belvoir, VA: Defense Technical Information Center, aprile 2007. http://dx.doi.org/10.21236/ada471495.

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Garlid, Anders. Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling? Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.1640.

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Smith, Samson. Effects of Reactive Oxygen Species on Life History Traits of Caenorhabditis elegans. Portland State University Library, gennaio 2000. http://dx.doi.org/10.15760/etd.712.

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Asenath-Smith, Emily, Emma Ambrogi, Eftihia Barnes e Jonathon Brame. CuO enhances the photocatalytic activity of Fe₂O₃ through synergistic reactive oxygen species interactions. Engineer Research and Development Center (U.S.), settembre 2021. http://dx.doi.org/10.21079/11681/42131.

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Abstract (sommario):
Iron oxide (α-Fe₂O₃, hematite) colloids were synthesized under hydrothermal conditions and investigated as catalysts for the photodegradation of an organic dye under broad-spectrum illumination. To enhance photocatalytic performance, Fe₂O₃ was combined with other transition-metal oxide (TMO) colloids (e.g., CuO and ZnO), which are sensitive to different regions of the solar spectrum (far visible and ultraviolet, respectively), using a ternary blending approach for compositional mixtures. For a variety of ZnO/Fe₂O₃/CuO mole ratios, the pseudo-first-order rate constant for methyl orange degradation was at least double the sum of the individual Fe₂O₃ and CuO rate constants, indicating there is an underlying synergy governing the photocatalysis reaction with these combinations of TMOs. A full compositional study was carried out to map the interactions between the three TMOs. Additional experiments probed the identity and role of reactive oxygen species and elucidated the mechanism by which CuO enhanced Fe₂O₃ photodegradation while ZnO did not. The increased photocatalytic performance of Fe2O3 in the presence of CuO was associated with hydroxyl radical ROS, consistent with heterogeneous photo-Fenton mechanisms, which are not accessible by ZnO. These results imply that low-cost photocatalytic materials can be engineered for high performance under solar illumination by selective pairing of TMOs with compatible ROS.
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Droby, Samir, Michael Wisniewski, Ron Porat e Dumitru Macarisin. Role of Reactive Oxygen Species (ROS) in Tritrophic Interactions in Postharvest Biocontrol Systems. United States Department of Agriculture, dicembre 2012. http://dx.doi.org/10.32747/2012.7594390.bard.

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To elucidate the role of ROS in the tri-trophic interactions in postharvest biocontrol systems a detailed molecular and biochemical investigation was undertaken. The application of the yeast biocontrol agent Metschnikowia fructicola, microarray analysis was performed on grapefruit surface wounds using an Affymetrix Citrus GeneChip. the data indicated that 1007 putative unigenes showed significant expression changes following wounding and yeast application relative to wounded controls. The expression of the genes encoding Respiratory burst oxidase (Rbo), mitogen-activated protein kinase (MAPK) and mitogen-activated protein kinase kinase (MAPKK), G-proteins, chitinase (CHI), phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS) and 4-coumarate-CoA ligase (4CL). In contrast, three genes, peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT), were down-regulated in grapefruit peel tissue treated with yeast cells. The yeast antagonists, Metschnikowia fructicola (strain 277) and Candida oleophila (strain 182) generate relatively high levels of super oxide anion (O2−) following its interaction with wounded fruit surface. Using laser scanning confocal microscopy we observed that the application of M. fructicola and C. oleophila into citrus and apple fruit wounds correlated with an increase in H2O2 accumulation in host tissue. The present data, together with our earlier discovery of the importance of H₂O₂ production in the defense response of citrus flavedo to postharvest pathogens, indicate that the yeast-induced oxidative response in fruit exocarp may be associated with the ability of specific yeast species to serve as biocontrol agents for the management of postharvest diseases. Effect of ROS on yeast cells was also studied. Pretreatment of the yeast, Candida oleophila, with 5 mM H₂O₂ for 30 min (sublethal) increased yeast tolerance to subsequent lethal levels of oxidative stress (50 mM H₂O₂), high temperature (40 °C), and low pH (pH 4). Suppression subtractive hybridization analysis was used to identify genes expressed in yeast in response to sublethal oxidative stress. Transcript levels were confirmed using semi quantitative reverse transcription-PCR. Seven antioxidant genes were up regulated. Pretreatment of the yeast antagonist Candida oleophila with glycine betaine (GB) increases oxidative stress tolerance in the microenvironment of apple wounds. ROS production is greater when yeast antagonists used as biocontrol agents are applied in the wounds. Compared to untreated control yeast cells, GB-treated cells recovered from the oxidative stress environment of apple wounds exhibited less accumulation of ROS and lower levels of oxidative damage to cellular proteins and lipids. Additionally, GB-treated yeast exhibited greater biocontrol activity against Penicillium expansum and Botrytis cinerea, and faster growth in wounds of apple fruits compared to untreated yeast. The expression of major antioxidant genes, including peroxisomal catalase, peroxiredoxin TSA1, and glutathione peroxidase was elevated in the yeast by GB treatment. A mild heat shock (HS) pretreatment (30 min at 40 1C) improved the tolerance of M. fructicola to subsequent high temperature (45 1C, 20–30 min) and oxidative stress (0.4 mol-¹) hydrogen peroxide, 20–60 min). HS-treated yeast cells showed less accumulation of reactive oxygen species (ROS) than non-treated cells in response to both stresses. Additionally, HS-treated yeast exhibited significantly greater (P≥0.0001) biocontrol activity against Penicillium expansum and a significantly faster (Po0.0001) growth rate in wounds of apple fruits stored at 25 1C compared with the performance of untreated yeast cells. Transcription of a trehalose-6-phosphate synthase gene (TPS1) was up regulated in response to HS and trehalose content also increased.
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Friedman, Haya, Chris Watkins, Susan Lurie e Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, dicembre 2009. http://dx.doi.org/10.32747/2009.7613883.bard.

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Abstract (sommario):
Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.
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Savory, John. Opening of the Mitochondrial Permeability Transition Pore by Reactive Oxygen Species is a Basic Event Neurodegeneration. Fort Belvoir, VA: Defense Technical Information Center, luglio 2001. http://dx.doi.org/10.21236/ada396332.

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Savory, John. Opening of the Mitochondrial Permeability Transition Pore by Reactive Oxygen Species is a Basic Event in Neurodegeneration. Fort Belvoir, VA: Defense Technical Information Center, luglio 2003. http://dx.doi.org/10.21236/ada418669.

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Liang, Feixin. Effect of reactive oxygen species on the ligand-independent activation of EGFR in tongue squamous cell carcinoma. Science Repository, giugno 2018. http://dx.doi.org/10.31487/j.dobcr.2018.02.005.

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