Journal articles: 'Cycle redox'

1

Wigginton, N. S. "The phosphorus redox cycle." Science 348, no. 6236 (May 14, 2015): 768. http://dx.doi.org/10.1126/science.348.6236.768-k.

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Diaz Vivancos, Pedro, Tonja Wolff, Jelena Markovic, Federico V. Pallardó, and Christine H. Foyer. "A nuclear glutathione cycle within the cell cycle." Biochemical Journal 431, no. 2 (September 28, 2010): 169–78. http://dx.doi.org/10.1042/bj20100409.

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The complex antioxidant network of plant and animal cells has the thiol tripeptide GSH at its centre to buffer ROS (reactive oxygen species) and facilitate cellular redox signalling which controls growth, development and defence. GSH is found in nearly every compartment of the cell, including the nucleus. Transport between the different intracellular compartments is pivotal to the regulation of cell proliferation. GSH co-localizes with nuclear DNA at the early stages of proliferation in plant and animal cells. Moreover, GSH recruitment and sequestration in the nucleus during the G1- and S-phases of the cell cycle has a profound impact on cellular redox homoeostasis and on gene expression. For example, the abundance of transcripts encoding stress and defence proteins is decreased when GSH is sequestered in the nucleus. The functions of GSHn (nuclear GSH) are considered in the present review in the context of whole-cell redox homoeostasis and signalling, as well as potential mechanisms for GSH transport into the nucleus. We also discuss the possible role of GSHn as a regulator of nuclear proteins such as histones and PARP [poly(ADP-ribose) polymerase] that control genetic and epigenetic events. In this way, a high level of GSH in the nucleus may not only have an immediate effect on gene expression patterns, but also contribute to how cells retain a memory of the cellular redox environment that is transferred through generations.

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Kang, Y. James. "Metallothionein Redox Cycle and Function." Experimental Biology and Medicine 231, no. 9 (October 2006): 1459–67. http://dx.doi.org/10.1177/153537020623100903.

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4

Bush, T., I. B. Butler, A. Free, and R. J. Allen. "Redox regime shifts in microbially mediated biogeochemical cycles." Biogeosciences 12, no. 12 (June 17, 2015): 3713–24. http://dx.doi.org/10.5194/bg-12-3713-2015.

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Abstract. Understanding how the Earth's biogeochemical cycles respond to environmental change is a prerequisite for the prediction and mitigation of the effects of anthropogenic perturbations. Microbial populations mediate key steps in these cycles, yet they are often crudely represented in biogeochemical models. Here, we show that microbial population dynamics can qualitatively affect the response of biogeochemical cycles to environmental change. Using simple and generic mathematical models, we find that nutrient limitations on microbial population growth can lead to regime shifts, in which the redox state of a biogeochemical cycle changes dramatically as the availability of a redox-controlling species, such as oxygen or acetate, crosses a threshold (a "tipping point"). These redox regime shifts occur in parameter ranges that are relevant to the present-day sulfur cycle in the natural environment and the present-day nitrogen cycle in eutrophic terrestrial environments. These shifts may also have relevance to iron cycling in the iron-containing Proterozoic and Archean oceans. We show that redox regime shifts also occur in models with physically realistic modifications, such as additional terms, chemical states, or microbial populations. Our work reveals a possible new mechanism by which regime shifts can occur in nutrient-cycling ecosystems and biogeochemical cycles, and highlights the importance of considering microbial population dynamics in models of biogeochemical cycles.

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5

Da Lozzo, Eneida Janiscki, Antonio Salvio Mangrich, Maria Eliane Merlin Rocha, Maria Benigna Martinelli de Oliveira, and Eva Gunilla Skare Carnieri. "Effects of citrinin on iron-redox cycle." Cell Biochemistry and Function 20, no. 1 (2002): 19–29. http://dx.doi.org/10.1002/cbf.931.

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Pasek, M. A., J. M. Sampson, and Z. Atlas. "Redox chemistry in the phosphorus biogeochemical cycle." Proceedings of the National Academy of Sciences 111, no. 43 (October 13, 2014): 15468–73. http://dx.doi.org/10.1073/pnas.1408134111.

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7

Sarsour, Ehab H., Amanda L. Kalen, and Prabhat C. Goswami. "Manganese Superoxide Dismutase Regulates a Redox Cycle Within the Cell Cycle." Antioxidants & Redox Signaling 20, no. 10 (April 2014): 1618–27. http://dx.doi.org/10.1089/ars.2013.5303.

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8

Foyer, Christine H., Michael H. Wilson, and Megan H. Wright. "Redox regulation of cell proliferation: Bioinformatics and redox proteomics approaches to identify redox-sensitive cell cycle regulators." Free Radical Biology and Medicine 122 (July 2018): 137–49. http://dx.doi.org/10.1016/j.freeradbiomed.2018.03.047.

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9

Hu, Min, Yuhong Zou, Shashank Manohar Nambiar, Joonyong Lee, Yan Yang, and Guoli Dai. "Keap1 modulates the redox cycle and hepatocyte cell cycle in regenerating liver." Cell Cycle 13, no. 15 (May 28, 2014): 2349–58. http://dx.doi.org/10.4161/cc.29298.

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10

Lau, Ka-Cheong, Ilya A. Shkrob, Nancy L. Dietz Rago, Justin G. Connell, Daniel Phelan, Bin Hu, Lu Zhang, Zhengcheng Zhang, and Chen Liao. "Improved performance through tight coupling of redox cycles of sulfur and 2,6-polyanthraquinone in lithium–sulfur batteries." Journal of Materials Chemistry A 5, no. 46 (2017): 24103–9. http://dx.doi.org/10.1039/c7ta08129d.

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11

Conour, J. E., W. V. Graham, and H. R. Gaskins. "A combined in vitro/bioinformatic investigation of redox regulatory mechanisms governing cell cycle progression." Physiological Genomics 18, no. 2 (July 8, 2004): 196–205. http://dx.doi.org/10.1152/physiolgenomics.00058.2004.

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The intracellular reduction-oxidation (redox) environment influences cell cycle progression; however, underlying mechanisms are poorly understood. To examine potential mechanisms, the intracellular redox environment was characterized per cell cycle phase in Chinese hamster ovary fibroblasts via flow cytometry by measuring reduced glutathione (GSH), reactive oxygen species (ROS), and DNA content with monochlorobimane, 2′,7′-dichlorohydrofluorescein diacetate (H2DCFDA), and DRAQ5, respectively. GSH content was significantly greater in G2/M compared with G1phase cells, whereas GSH was intermediate in S phase cells. ROS content was similar among phases. Together, these data demonstrate that G2/M cells are more reduced than G1cells. Conventional approaches to define regulatory mechanisms are subjective in nature and focus on single proteins/pathways. Proteome databases provide a means to overcome these inherent limitations. Therefore, a novel bioinformatic approach was developed to exhaustively identify putative redox-regulated cell cycle proteins containing redox-sensitive protein motifs. Using the InterPro ( http://www.ebi.ac.uk/interpro/ ) database, we categorized 536 redox-sensitive motifs as: 1) active/functional-site cysteines, 2) electron transport, 3) heme, 4) iron binding, 5) zinc binding, 6) metal binding (non-Fe/Zn), and 7) disulfides. Comparing this list with 1,634 cell cycle-associated proteins from Swiss-Prot and SpTrEMBL ( http://us.expasy.org/sprot/ ) revealed 92 candidate proteins. Three-fourths (69 of 92) of the candidate proteins function in the central cell cycle processes of transcription, nucleotide metabolism, (de)phosphorylation, and (de)ubiquitinylation. The majority of oxidant-sensitive candidate proteins (68.9%) function during G2/M phase. As the G2/M phase is more reduced than the G1phase, oxidant-sensitive proteins may be temporally regulated by oscillation of the intracellular redox environment. Combined with evidence of intracellular redox compartmentalization, we propose a spatiotemporal mechanism that functionally links an oscillating intracellular redox environment with cell cycle progression.

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12

Bogdanovic, Visnja, and Mihajlo Spasic. "Redox regulation of cell cycle through nitric oxide." Chemical Industry 62, no. 5 (2008): 301–4. http://dx.doi.org/10.2298/hemind0805301b.

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This paper investigates the effects of sodium nitroprusside as NO donor on two cell lines in culture: transformed cells of mice fibroblasts (L929) and malignant cells of human eritroleukemia (K562). Low concentrations of NO have stimulative effect, while high concentrations have inhibitive effects on proliferation of K562 cells in a dose-dependent manner. In our experiments, by using sodium nitroprusside (SNP) as NO donor and two kinds of superoxide dismutase, Cu,Zn-SOD and Mn-SOD, we created conditions to generate several kinds of signal molecules and investigated reaction of transformed (L929) and malignant (K562) cells to dose. Results of experiments are showing that chosen parameters (amount of free thiol groups and glutathione) may be relevant in monitoring the effect of exogenous nitrate oxide and its redox descendants in different, both transformed and malignant cell lines.

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13

Scheffe, Jonathan R., Jianhua Li, and Alan W. Weimer. "A spinel ferrite/hercynite water-splitting redox cycle." International Journal of Hydrogen Energy 35, no. 8 (April 2010): 3333–40. http://dx.doi.org/10.1016/j.ijhydene.2010.01.140.

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14

Wang, Haojie, Han Ding, Benhua Ma, and Zhijun Chen. "A redox cycle meets insulin fibrillation in vitro." International Journal of Biological Macromolecules 138 (October 2019): 89–96. http://dx.doi.org/10.1016/j.ijbiomac.2019.07.002.

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15

Sheu, Elysia J., Esmail M. A. Mokheimer, and Ahmed F. Ghoniem. "Dry redox reforming hybrid power cycle: Performance analysis and comparison to steam redox reforming." International Journal of Hydrogen Energy 40, no. 7 (February 2015): 2939–49. http://dx.doi.org/10.1016/j.ijhydene.2015.01.018.

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16

Strange, Charlie, Andrew Gottehrer, Karen Birmingham, and John E. Heffner. "Platelets attenuate oxidant-induced permeability in endothelial monolayers: glutathione-dependent mechanisms." Journal of Applied Physiology 81, no. 4 (October 1, 1996): 1701–6. http://dx.doi.org/10.1152/jappl.1996.81.4.1701.

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Strange, Charlie, Andrew Gottehrer, Karen Birmingham, and John E. Heffner. Platelets attenuate oxidant-induced permeability in endothelial monolayers: glutathione-dependent mechanisms. J. Appl. Physiol. 81(4): 1701–1706, 1996.—We studied the effects of adding washed human platelets or platelets with nonintact glutathione redox cycles to endothelial cell monolayers treated with glucose oxidase to initiate oxidant stress and increase permeability. Changes in125I-labeled albumin transmonolayer movement were used as the index of monolayer permeability. Washed human platelets attenuated oxidant-induced increases in albumin flux. Platelets treated with 1,3-bis(2-chloroethyl)-1-nitrosurea, 1-chloro-2,4-dinitrobenzene, or buthionine sulfoximine to inhibit selective enzymatic steps in the glutathione redox cycle decreased permeability to a lesser degree. We conclude that 1) washed human platelets attenuate monolayer permeability defects in aortic endothelial monolayers exposed to glucose oxidase and 2) the protective effects of platelets are partially dependent on an intact platelet glutathione redox cycle.

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17

Rani, Pallavi, Suman Kumari Jhajharia, and Kaliaperumal Selvaraj. "A redox-mediated 3D graphene based nanoscoop design for ultracapacitor applications." New Journal of Chemistry 41, no. 16 (2017): 8390–98. http://dx.doi.org/10.1039/c7nj01461a.

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The judicious design of 3D graphene with a unique nanostructure blended with an active redox species demonstrates the ability to boost capacitance as high as 8-fold. This design not only exhibits high specific capacitance but also sustains it with a good cycle stability of even beyond 5000 cycles.

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18

Bush, T., I. B. Butler, A. Free, and R. J. Allen. "Redox regime shifts in microbially-mediated biogeochemical cycles." Biogeosciences Discussions 12, no. 4 (February 17, 2015): 3283–314. http://dx.doi.org/10.5194/bgd-12-3283-2015.

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Abstract. Understanding how the Earth's biogeochemical cycles respond to environmental change is a prerequisite for the prediction and mitigation of the effects of anthropogenic perturbations. Microbial populations mediate key steps in these cycles, yet are often crudely represented in biogeochemical models. Here, we show that microbial population dynamics can qualitatively affect the response of biogeochemical cycles to environmental change. Using simple and generic mathematical models, we find that nutrient limitations on microbial population growth can lead to regime shifts, in which the redox state of a biogeochemical cycle changes dramatically as the availability of a redox-controlling species, such as oxygen or acetate, crosses a threshold (a "tipping point"). These redox regime shifts occur in parameter ranges that are relevant to the sulfur and nitrogen cycles in the present-day natural environment, and may also have relevance to iron cycling in the iron-containing Proterozoic and Archean oceans. We show that redox regime shifts also occur in models with physically realistic modifications, such as additional terms, chemical states, or microbial populations. Our work reveals a possible new mechanism by which regime shifts can occur in nutrient-cycling ecosystems and biogeochemical cycles, and highlights the importance of considering microbial population dynamics in models of biogeochemical cycles.

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19

Kim, Mi-Lim, and Kyung-Ho Choi. "Effect of Herbicide Paraquat on NAD(H)-Redox-cycle." Journal of Life Science 15, no. 2 (April 1, 2005): 304–10. http://dx.doi.org/10.5352/jls.2005.15.2.304.

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20

Clay, D. E., J. A. E. Molina, C. E. Clapp, and D. R. Linden. "Soil Tillage Impact on the Diurnal Redox-Potential Cycle." Soil Science Society of America Journal 54, no. 2 (March 1990): 516–21. http://dx.doi.org/10.2136/sssaj1990.03615995005400020038x.

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21

Weber, Selina, Jens F. Peters, Manuel Baumann, and Marcel Weil. "Life Cycle Assessment of a Vanadium Redox Flow Battery." Environmental Science & Technology 52, no. 18 (August 22, 2018): 10864–73. http://dx.doi.org/10.1021/acs.est.8b02073.

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22

Ma, Ling Juan, Lin Shen Chen, and Song Ying Chen. "Studies on redox H2–CO2 cycle on CoCrxFe2−xO4." Solid State Sciences 11, no. 1 (January 2009): 176–81. http://dx.doi.org/10.1016/j.solidstatesciences.2008.05.008.

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23

Rothstein, Emily C., and Pamela A. Lucchesi. "Redox Control of the Cell Cycle: A Radical Encounter." Antioxidants & Redox Signaling 7, no. 5-6 (May 2005): 701–3. http://dx.doi.org/10.1089/ars.2005.7.701.

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24

KUMADA, Keigo, Kazuhisa SATO, and Toshiyuki HASHIDA. "Investigation into Degradations of SOFCs under Redox Cycle Environments." Proceedings of Autumn Conference of Tohoku Branch 2017.53 (2017): 114. http://dx.doi.org/10.1299/jsmetohoku.2017.53.114.

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25

Kishi, Takeo, Takayuki Takahashi, Akinori Usui, and Tadashi Okamoto. "Ubiquinone redox cycle as a cellular antioxidant defense system." BioFactors 10, no. 2-3 (1999): 131–38. http://dx.doi.org/10.1002/biof.5520100208.

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26

Kakkar, Rita, and Mamta Bhandari. "Theoretical investigation of the alloxan-dialuric acid redox cycle." International Journal of Quantum Chemistry 113, no. 17 (March 23, 2013): 2060–69. http://dx.doi.org/10.1002/qua.24441.

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27

Rana, Payal, Russell Naven, Arjun Narayanan, Yvonne Will, and Lyn H. Jones. "Chemical motifs that redox cycle and their associated toxicity." MedChemComm 4, no. 8 (2013): 1175. http://dx.doi.org/10.1039/c3md00149k.

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28

Hayes, John M., and Jacob R. Waldbauer. "The carbon cycle and associated redox processes through time." Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1470 (May 8, 2006): 931–50. http://dx.doi.org/10.1098/rstb.2006.1840.

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Earth's biogeochemical cycle of carbon delivers both limestones and organic materials to the crust. In numerous, biologically catalysed redox reactions, hydrogen, sulphur, iron, and oxygen serve prominently as electron donors and acceptors. The progress of these reactions can be reconstructed from records of variations in the abundance of 13 C in sedimentary carbonate minerals and organic materials. Because the crust is always receiving new CO 2 from the mantle and a portion of it is being reduced by photoautotrophs, the carbon cycle has continuously released oxidizing power. Most of it is represented by Fe 3+ that has accumulated in the crust or been returned to the mantle via subduction. Less than 3% of the estimated, integrated production of oxidizing power since 3.8 Gyr ago is represented by O 2 in the atmosphere and dissolved in seawater. The balance is represented by sulphate. The accumulation of oxidizing power can be estimated from budgets summarizing inputs of mantle carbon and rates of organic-carbon burial, but levels of O 2 are only weakly and indirectly coupled to those phenomena and thus to carbon-isotopic records. Elevated abundances of 13 C in carbonate minerals ca 2.3 Gyr old, in particular, are here interpreted as indicating the importance of methanogenic bacteria in sediments rather than increased burial of organic carbon.

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29

Vener, Alexander V., Paul J. M. van Kan, Alma Gal, Bertil Andersson, and Itzhak Ohad. "Activation/Deactivation Cycle of Redox-controlled Thylakoid Protein Phosphorylation." Journal of Biological Chemistry 270, no. 42 (October 20, 1995): 25225–32. http://dx.doi.org/10.1074/jbc.270.42.25225.

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30

Amini, Kiana, and Mark D. Pritzker. "Life-cycle analysis of zinc-cerium redox flow batteries." Electrochimica Acta 356 (October 2020): 136785. http://dx.doi.org/10.1016/j.electacta.2020.136785.

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31

Chaiswing, Luksana, Chontida Yarana, Dustin Carroll, Michael Alstott, Allan Butterfield, Subbarao Bondada, Ines Batinic-Haber, Ivan Spasojevic, and Daret St Clair. "Redox State Determines the Differential Effects of Redox-Cycle Compounds in Chemoresistant Ovarian Cancer Cells." Free Radical Biology and Medicine 112 (November 2017): 86. http://dx.doi.org/10.1016/j.freeradbiomed.2017.10.124.

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32

Huang, Peng, Wei Ling, Hang Sheng, Yan Zhou, Xiaopeng Wu, Xian-Xiang Zeng, Xiongwei Wu, and Yu-Guo Guo. "Heteroatom-doped electrodes for all-vanadium redox flow batteries with ultralong lifespan." Journal of Materials Chemistry A 6, no. 1 (2018): 41–44. http://dx.doi.org/10.1039/c7ta07358e.

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The heteroatom-doped graphite felt electrode with prominent hydrophilicity presents excellent electroactivity towards V²⁺/V³⁺ and VO²⁺/VO₂⁺, and dramatically extends the energy efficiency of vanadium redox flow batteries towards 1000 cycles with 0.003% reduction per cycle.

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33

Menon, S. G., and P. C. Goswami. "A redox cycle within the cell cycle: ring in the old with the new." Oncogene 26, no. 8 (August 21, 2006): 1101–9. http://dx.doi.org/10.1038/sj.onc.1209895.

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34

Banjac, A., T. Perisic, H. Sato, A. Seiler, S. Bannai, N. Weiss, P. Kölle, et al. "The cystine/cysteine cycle: a redox cycle regulating susceptibility versus resistance to cell death." Oncogene 27, no. 11 (September 10, 2007): 1618–28. http://dx.doi.org/10.1038/sj.onc.1210796.

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35

Burhans, William C., and Nicholas H. Heintz. "The cell cycle is a redox cycle: Linking phase-specific targets to cell fate." Free Radical Biology and Medicine 47, no. 9 (November 2009): 1282–93. http://dx.doi.org/10.1016/j.freeradbiomed.2009.05.026.

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36

Cardaci, Simone, and Maria Rosa Ciriolo. "TCA Cycle Defects and Cancer: When Metabolism Tunes Redox State." International Journal of Cell Biology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/161837.

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Inborn defects of the tricarboxylic acid (TCA) cycle enzymes have been known for more than twenty years. Until recently, only recessive mutations were described which, although resulted in severe multisystem syndromes, did not predispose to cancer onset. In the last ten years, a causal role in carcinogenesis has been documented for inherited and acquired alterations in three TCA cycle enzymes, succinate dehydrogenase (SDH), fumarate hydratase (FH), and isocitrate dehydrogenase (IDH), pointing towards metabolic alterations as the underlying hallmark of cancer. This paper summarizes the neoplastic alterations of the TCA cycle enzymes focusing on the generation of pseudohypoxic phenotype and the alteration of epigenetic homeostasis as the main tumor-promoting effects of the TCA cycle affecting defects. Moreover, we debate on the ability of these mutations to affect cellular redox state and to promote carcinogenesis by impacting on redox biology.

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37

Suttorp, N., W. Toepfer, and L. Roka. "Antioxidant defense mechanisms of endothelial cells: glutathione redox cycle versus catalase." American Journal of Physiology-Cell Physiology 251, no. 5 (November 1, 1986): C671—C680. http://dx.doi.org/10.1152/ajpcell.1986.251.5.c671.

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The importance of the glutathione (GSH) redox cycle and of catalase as intracellular antioxidant defense systems in cultured endothelial cells against an extracellular flux of H2O2, a critical mediator of polymorphonuclear leukocyte-induced oxidant injury of endothelial cells, was examined. The activities of different parts of the GSH redox cycle were impaired by 1,3-bis(2-chloroethyl)-1-nitrosourea, buthionine sulfoximine, diethyl maleate and 2-cyclohexene-1-one. Catalase activity was inhibited by 3-amino-1,2,4-triazole. After an impairment of the GSH redox cycle, but not of catalase, the susceptibility of pulmonary artery endothelial cells to an attack by H2O2 was dramatically increased independent of the source of extracellularly generated hydrogen peroxide (i.e., glucose oxidase or stimulated polymorphonuclear leukocytes). Exogenous catalase, d-alpha-tocopherol, and particularly Trolox, the chroman compound of tocopherol, but not phytol, the fatty acid side chain of tocopherol, provided almost complete protection of the endothelial cells against a H2O2-mediated attack. Additional fluorometric studies suggested that H2O2 is scavenged by the antioxidants before it hits the target cells.

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Carrillo, A. J., D. Sastre, D. P. Serrano, P. Pizarro, and J. M. Coronado. "Revisiting the BaO2/BaO redox cycle for solar thermochemical energy storage." Physical Chemistry Chemical Physics 18, no. 11 (2016): 8039–48. http://dx.doi.org/10.1039/c5cp07777j.

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Zhang, Jingjing, Jinhua Huang, Lily A. Robertson, Ilya A. Shkrob, and Lu Zhang. "Comparing calendar and cycle life stability of redox active organic molecules for nonaqueous redox flow batteries." Journal of Power Sources 397 (September 2018): 214–22. http://dx.doi.org/10.1016/j.jpowsour.2018.07.001.

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40

Eckert, W., and H. G. Trüper. "Microbially — related redox changes in a subtropical lake I.In situ monitoring of the annual redox cycle." Biogeochemistry 21, no. 1 (March 1993): 1–19. http://dx.doi.org/10.1007/bf00002685.

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41

Zhelev, Zhivko, Ichio Aoki, Veselina Gadjeva, Biliana Nikolova, Rumiana Bakalova, and Tsuneo Saga. "Tissue redox activity as a sensing platform for imaging of cancer based on nitroxide redox cycle." European Journal of Cancer 49, no. 6 (April 2013): 1467–78. http://dx.doi.org/10.1016/j.ejca.2012.10.026.

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42

Macnab, Andrew J., Roy E. Gagnon, Faith A. Gagnon, Derek Blackstock, and Jacques G. LeBlanc. "Cardiac Bypass Pump Flow Management via NIRS Monitoring." Spectroscopy 17, no. 2-3 (2003): 477–82. http://dx.doi.org/10.1155/2003/693192.

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During cardiac surgery, bypass pumps rely on pressure monitors to evaluate flow. We studied whether it would be possible to optimize pump flow by monitoring changes in cerebral cytochromea,a3using NIRS to maintain cyt redox status at its pre-bypass level.Method: 18 healthy 7–45 kg swine were placed on bypass for repeated cycles of cooling and re-warming from 36 to 15 to 36°C in 3°C steps. Between each cycle, the swine's bypass pump blood flow rate was adjusted to restore cytochrome redox status to its pre-bypass value.Results: In all swine trials, the number of pump flow alterations imposed by NIRS monitoring ranged from 0 to 42, the average being 14 per trial. The best trial had 22 pump flow adjustments during which the range of cytochrome redox status change was 0.50±0.06μmol l–1. The average trial had a range of cytochrome redox status change of 1.50±0.22μmol l–1.Conclusion: NIRS-driven alterations in pump flow rate to maintain pre-bypass cytochrome redox status can be achieved successfully in the animal model.

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43

Wei, Yong Gang, Xing Zhu, Kong Zhai Li, Ya Ne Zheng, and Hua Wang. "Reaction Characteristics of Ce-Based Oxygen Carrier for Two-Step Production Syngas and Hydrogen through Methane Conversion and Water Splitting." Advanced Materials Research 641-642 (January 2013): 123–27. http://dx.doi.org/10.4028/www.scientific.net/amr.641-642.123.

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The two-step steam methane reforming for production syngas and hydrogen was investigated by using Ce-based oxygen carriers (CeO2, CeO2-ZrO2，CeO2-Fe2O3) which were prepared by co-precipitation method and characterized by means of X-ray diffractometer and Raman spectroscopy. CH4 temperature programmed and isothermal reactions were adopted to test syngas production reactivity, and redox properties were evaluated by a successive redox cycle. The results showed that the incorporation of ZrO2 into CeO2 was found to be an effective approach for enhancing the reducibility of CeO2 in methane conversion reaction and redox performance, and the addition of Fe2O3 into CeO2 could obviously increase the amount of reactive oxygen species in CeO2-Fe2O3 and the yields of syngas and hydrogen reached maximum in the 3rd cycle, but the redox stability of CeO2-Fe2O3 needs to be enhanced.

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44

Shakhristova, Evgeniya V., Elena A. Stepovaya, Evgeniy V. Rudikov, Olga S. Sushitskaya, Daria O. Rodionova, and Vaycheslav V. Novitsky. "The Role of Redox Proteins in Arresting Proliferation of Breast Epithelial Cells Under Oxidative Stress." Annals of the Russian academy of medical sciences 73, no. 5 (October 25, 2018): 289–93. http://dx.doi.org/10.15690/vramn1030.

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Background: Redox status imbalance against the backdrop of oxidative stress development underlies the pathogenesis of a whole range of diseases. Many intracellular proteins contain free thiol groups and undergo redox regulation which is one of the key processes in controlling cell proliferation. Thioredoxin and glutaredoxin are involved in maintaining intracellular redox homeostasis and act as candidates in regulating proliferation. This provides prospects for future development of methods for diagnosis and targeted therapy of socially sensitive diseases accompanied by oxidative stress. The aim of the study is to reveal the role of redox proteins in molecular mechanisms of regulating HBL-100 breast epithelial cell proliferation under the effect of roscovitine, a cell cycle inhibitor. Materials and methods: Two research groups were formed. They included HBL-100 human breast epithelial cells incubated in the presence and absence of 20 mcM roscovitine for 18 hours. The intracellular thioredoxin levels were determined using Western blot analysis with specific monoclonal antibodies. Distribution of the cells among cell cycle phases were evaluated by flow cytometry. The activity of glutathione reductase, glutathione peroxidase, and thioredoxin reductase were measured by spectrophotometry. Results: Under the effect of roscovitine in the HBL-100 cells, cell cycle arrest in the G2/М phases occurred and oxidative stress developed. In the meantime, the decrease in the thioredoxin and glutaredoxin concentrations was registered along with the change in the functional activity of glutathione-dependent enzymes. Conclusions: Application of roscovitine, a cell cycle inhibitor, allowed creating a model of oxidative stress in the breast epithelial cells against the backdrop of inhibited cell proliferation. We identified that thioredoxin and glutaredoxin contributed to impairment of cell cycle progression. It points at a possibility to regulate cell proliferation by modulating the functional features of cellular redox-dependent proteins in different pathologies accompanied by oxidative stress.

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Silitonga, Septiani, Ricky Therisno, Richard A. M. Napitupulu, Charles S. P. Manurung, Parulian Siagian, and Yong Song Chen. "Redox Flow Battery Sebagai Perangkat Penyimpanan Energi." SPROCKET JOURNAL OF MECHANICAL ENGINEERING 2, no. 2 (February 26, 2021): 63–71. http://dx.doi.org/10.36655/sproket.v2i2.529.

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Energy storage such as vanadium redox flow batteries (VRFB) has increased to store renewable energy resources in the last decade. However, the unbalanced crossover level of vanadium is often a major constraint which has a significant impact on battery capacity and life cycle in long-term operation. Performing an asymmetric electrolyte volume is one of many ways to solve this problem. The different volumes on the positive and negative sides were analyzed to see their effect in suppressing the decrease in VRFB capacity. With the result of the optimal electrolyte excess ratio, long-term cycle performance was carried out to investigate the reduction in capacity of VRFBs.

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Shen, Wei Hua, and Shuichi Naito. "Easy Precipitation Method for Preparation of Cerium Added La₂O₂SO₄ Used for Oxygen Storage." Advanced Materials Research 886 (January 2014): 196–99. http://dx.doi.org/10.4028/www.scientific.net/amr.886.196.

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The present work gives a simple precipitation method for preparation of lanthanum oxysulfate and cerium modified lanthanum oxysulfate by using lanthanum nitrate and ammonium sulfate as precursor in the presence of ammonia. The XRD, TEM, XPS, and N2 sorption measurements have been adopted to characterize those materials. The present work demonstrates that cerium addition can promote the oxidation and reduction process between lanthanum oxysulfide (La2O2S) and lanthanum oxysulfate (La2O2SO4). The cerium doped La2O2SO4/La2O2S oxygen storage system showed the replacement of cerium for some La site to form a stable structure and no sulfur leakage took place in the process of redox cycle. The oxidation temperatures of Ln2O2S to Ln2O2SO4 decrease more than 150 °C for cerium doping samples; and the reduction temperature of La2O2SO4 to La2O2S in hydrogen decreases about 50 °C. The redox cycle between Ce3+ and Ce4+ has been considered response to the promotion of the redox cycle.

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Lu, Qi, Frances L. Jourd'heuil, and David Jourd'heuil. "Redox control of G1/S cell cycle regulators during nitric oxide-mediated cell cycle arrest." Journal of Cellular Physiology 212, no. 3 (2007): 827–39. http://dx.doi.org/10.1002/jcp.21079.

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Sankarasubramanian, Shrihari, Yunzhu Zhang, and Vijay Ramani. "Methanesulfonic acid-based electrode-decoupled vanadium–cerium redox flow battery exhibits significantly improved capacity and cycle life." Sustainable Energy & Fuels 3, no. 9 (2019): 2417–25. http://dx.doi.org/10.1039/c9se00286c.

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V–Ce RFBs (∼100% CE and ∼70% EE over 100 cycles) using a CH₃SO₃H-based electrolyte and a AEM separator shows 30% higher capacity and 0.024% capacity fade/cycle vs. 5% capacity fade/cycle for H₂SO₄ supported V–Ce ED-RFBs.

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Shakhristova, E. V., E. A. Stepovaya, A. A. Sadykova, and V. V. Novitsky. "Protein carbonylation as a possible way to modulate breast cancer cell proliferation." Siberian journal of oncology 17, no. 6 (January 1, 2019): 78–83. http://dx.doi.org/10.21294/1814-4861-2018-17-6-78-83.

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Introduction.High rates of cancer incidence and mortality worldwide dictate the necessity of developing new methodological approaches in understanding the molecular mechanisms of cancer progression associated with intracellular redox regulation imbalance.The objectiveof the study was to evaluate the role of protein carbonylation in regulating breast cancer cell proliferation under redox status modulation.Materials and Methods. In the intact breast cancer cells and in the cells cultured under redox status modulation using 5mM N-ethylmaleimide (an - SH group blocker) and 5 Mm 1,4-dithioerythritol (a thiol group protector), the concentration of thioredoxin and its carbonylated form was measured using Western blot analysis. The activity of thioredoxin reductase and the level of protein carbonyl derivatives were determined using spectrophotometry. Cell cycle phase distribution was evaluated by flow cytometry.Results and Discussion. Under the effect of N-ethylmaleimide, cell cycle arrest in the S-phase was confirmed by oxidative modification of proteins, including thioredoxin carbonylation. When culturing MCF-7 cells in the presence of 1,4-dithioerythritol, cell cycle arrest in the G0/G1 phases was associated with a rise in the concentrations of reduced thioredoxin and glutathione forms.Conclusion.The thioredoxin system and oxidative modification of proteins are involved in redox-dependent modulation of breast cancer cell proliferation. Studies in the area of redox proteomics offer great potential to seek molecular targets of malignant transformation of breast cells.

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Qin, Kaiqiang, Kathryn Holguin, Motahareh Mohammadiroudbari, and Chao Luo. "A conjugated tetracarboxylate anode for stable and sustainable Na-ion batteries." Chemical Communications 57, no. 19 (2021): 2360–63. http://dx.doi.org/10.1039/d0cc08273b.

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A conjugated tetracarboxylate, Na₄C₁₀H₂O₈, shows low redox potentials (∼0.65 V), long cycle life (1000 cycles), and fast charging capability (up to 2 A g⁻¹), demonstrating a promising organic anode for stable and sustainable Na-ion batteries.

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Journal articles on the topic 'Cycle redox'

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