Gotowe bibliografie tematyczne / Mitochondrial reactive oxygen species

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
  6. Raporty organizacyjne

Gotowa bibliografia na temat „Mitochondrial reactive oxygen species”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 19 lutego 2022

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Artykuły w czasopismach na temat "Mitochondrial reactive oxygen species"

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Murphy, Michael P. "How mitochondria produce reactive oxygen species." Biochemical Journal 417, no. 1 (December 12, 2008): 1–13. http://dx.doi.org/10.1042/bj20081386.

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The production of ROS (reactive oxygen species) by mammalian mitochondria is important because it underlies oxidative damage in many pathologies and contributes to retrograde redox signalling from the organelle to the cytosol and nucleus. Superoxide (O2•−) is the proximal mitochondrial ROS, and in the present review I outline the principles that govern O2•− production within the matrix of mammalian mitochondria. The flux of O2•− is related to the concentration of potential electron donors, the local concentration of O2 and the second-order rate constants for the reactions between them. Two mod
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Zorov, Dmitry B., Magdalena Juhaszova, and Steven J. Sollott. "Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release." Physiological Reviews 94, no. 3 (July 2014): 909–50. http://dx.doi.org/10.1152/physrev.00026.2013.

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Byproducts of normal mitochondrial metabolism and homeostasis include the buildup of potentially damaging levels of reactive oxygen species (ROS), Ca2+, etc., which must be normalized. Evidence suggests that brief mitochondrial permeability transition pore (mPTP) openings play an important physiological role maintaining healthy mitochondria homeostasis. Adaptive and maladaptive responses to redox stress may involve mitochondrial channels such as mPTP and inner membrane anion channel (IMAC). Their activation causes intra- and intermitochondrial redox-environment changes leading to ROS release.
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Zorov, Dmitry B., Charles R. Filburn, Lars-Oliver Klotz, Jay L. Zweier, and Steven J. Sollott. "Reactive Oxygen Species (Ros-Induced) Ros Release." Journal of Experimental Medicine 192, no. 7 (October 2, 2000): 1001–14. http://dx.doi.org/10.1084/jem.192.7.1001.

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We sought to understand the relationship between reactive oxygen species (ROS) and the mitochondrial permeability transition (MPT) in cardiac myocytes based on the observation of increased ROS production at sites of spontaneously deenergized mitochondria. We devised a new model enabling incremental ROS accumulation in individual mitochondria in isolated cardiac myocytes via photoactivation of tetramethylrhodamine derivatives, which also served to report the mitochondrial transmembrane potential, ΔΨ. This ROS accumulation reproducibly triggered abrupt (and sometimes reversible) mitochondrial de
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Camello-Almaraz, Cristina, Pedro J. Gomez-Pinilla, Maria J. Pozo, and Pedro J. Camello. "Mitochondrial reactive oxygen species and Ca2+ signaling." American Journal of Physiology-Cell Physiology 291, no. 5 (November 2006): C1082—C1088. http://dx.doi.org/10.1152/ajpcell.00217.2006.

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Mitochondria are an important source of reactive oxygen species (ROS) formed as a side product of oxidative phosphorylation. The main sites of oxidant production are complex I and complex III, where electrons flowing from reduced substrates are occasionally transferred to oxygen to form superoxide anion and derived products. These highly reactive compounds have a well-known role in pathological states and in some cellular responses. However, although their link with Ca2+ is well studied in cell death, it has been hardly investigated in normal cytosolic calcium concentration ([Ca2+]i) signals.
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Degli Esposti, M. "Measuring mitochondrial reactive oxygen species." Methods 26, no. 4 (April 2, 2002): 335–40. http://dx.doi.org/10.1016/s1046-2023(02)00039-7.

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Yoboue, Edgar D., and Anne Devin. "Reactive Oxygen Species-Mediated Control of Mitochondrial Biogenesis." International Journal of Cell Biology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/403870.

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Mitochondrial biogenesis is a complex process. It necessitates the contribution of both the nuclear and the mitochondrial genomes and therefore crosstalk between the nucleus and mitochondria. It is now well established that cellular mitochondrial content can vary according to a number of stimuli and physiological states in eukaryotes. The knowledge of the actors and signals regulating the mitochondrial biogenesis is thus of high importance. The cellular redox state has been considered for a long time as a key element in the regulation of various processes. In this paper, we report the involvem
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Richter, Christoph. "Reactive Oxygen and Nitrogen Species Regulate Mitochondrial Ca2+ Homeostasis and Respiration." Bioscience Reports 17, no. 1 (February 1, 1997): 53–66. http://dx.doi.org/10.1023/a:1027387301845.

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The reduction of molecular oxygen to water provides most of the biologically useful energy. However, oxygen reduction is a mixed blessing because incompletely reduced oxygen species such as superoxide or peroxides are quite reactive and can, when out of control, cause damage. In mitochondria, where most of the oxygen utilized by eukaryotic cells is reduced, the dichotomy of oxygen shows itself best. Thus, reactive oxygen is a threat to them, as is evident from oxidative damage to mitochondrial lipids, proteins, and nucleic acids. Reactive oxygen, in the form of peroxides, also serves useful fu
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Zhang, David X., and David D. Gutterman. "Mitochondrial reactive oxygen species-mediated signaling in endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (May 2007): H2023—H2031. http://dx.doi.org/10.1152/ajpheart.01283.2006.

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Once thought of as toxic by-products of cellular metabolism, reactive oxygen species (ROS) have been implicated in a large variety of cell-signaling processes. Several enzymatic systems contribute to ROS production in vascular endothelial cells, including NA(D)PH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase, and the mitochondrial electron transport chain. The respiratory chain is the major source of ROS in most mammalian cells, but the role of mitochondria-derived ROS in vascular cell signaling has received little attention. A new paradigm has evolved in recent years
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Mailloux, Ryan J. "An Update on Mitochondrial Reactive Oxygen Species Production." Antioxidants 9, no. 6 (June 2, 2020): 472. http://dx.doi.org/10.3390/antiox9060472.

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Mitochondria are quantifiably the most important sources of superoxide (O2●−) and hydrogen peroxide (H2O2) in mammalian cells. The overproduction of these molecules has been studied mostly in the contexts of the pathogenesis of human diseases and aging. However, controlled bursts in mitochondrial ROS production, most notably H2O2, also plays a vital role in the transmission of cellular information. Striking a balance between utilizing H2O2 in second messaging whilst avoiding its deleterious effects requires the use of sophisticated feedback control and H2O2 degrading mechanisms. Mitochondria a
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Nethery, D., L. A. Callahan, D. Stofan, R. Mattera, A. DiMarco, and G. Supinski. "PLA2dependence of diaphragm mitochondrial formation of reactive oxygen species." Journal of Applied Physiology 89, no. 1 (July 1, 2000): 72–80. http://dx.doi.org/10.1152/jappl.2000.89.1.72.

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Contraction-induced respiratory muscle fatigue and sepsis-related reductions in respiratory muscle force-generating capacity are mediated, at least in part, by reactive oxygen species (ROS). The subcellular sources and mechanisms of generation of ROS in these conditions are incompletely understood. We postulated that the physiological changes associated with muscle contraction (i.e., increases in calcium and ADP concentration) stimulate mitochondrial generation of ROS by a phospholipase A2(PLA2)-modulated process and that sepsis enhances muscle generation of ROS by upregulating PLA2activity. T
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Rozprawy doktorskie na temat "Mitochondrial reactive oxygen species"

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

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

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This work investigates the reactions of proteins with ROS when mitochondria are exposed to H<sub>2</sub>O<sub>2</sub> or when they generate ROS endogenously. Using isolated mitochondria, those proteins that are particularly sensitive to low concentrations of H<sub>2</sub>O<sub>2</sub> and to ROS generated by the mitochondrial electron transport chain were first identified using a method called Redox-Difference Gel Electrophoresis (Redox-DIGE). Most redox sensitive thiol proteins identified by Redox-DIGE were involved either in fatty acid oxidation or in the regulation of the pyruvate dehydroge
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Li, Xinyuan. "Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/320473.

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Pharmacology<br>Ph.D.<br>Lysophosphatidylcholines (LPCs) are a class of pro-inflammatory lipids that play important roles in atherogenesis. LPC activates endothelial cells (ECs) to upregulate adhesion molecules, cytokines and chemokines, which is the initiation step of atherogenesis. However, the mechanisms underlying LPC-triggered EC activation are not fully understood. Previously considered as the toxic by-products of cellular metabolism, mitochondrial reactive oxygen species (mtROS) are recently found to directly contribute to both the innate and adaptive immune responses. Here we tested a
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Hinchy, Elizabeth. "How cellular ATP/ADP ratios and reactive oxygen species affect AMPK signalling." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270029.

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Mitochondria are key generators of cellular ATP, vital to complex life. Historically, mitochondrial generation of reactive oxygen species (ROS) was considered to be an unregulated process, produced by dysfunctional mitochondria. More recently, mitochondrial ROS generated by complex I, particularly by the process of reverse electron transfer (RET), has emerged as a potentially biologically relevant signal that is tightly-regulated and dependent on mitochondrial status. ROS production by RET is reported to play a role in the innate immune response and lifespan extension in fruit flies. One way i
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Collins, Yvonne. "Regulation of pyruvate dehydrogenase kinase 2 by mitochondrial reactive oxygen species." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708470.

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

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Ageing is a risk factor for the development of cardiovascular disease. In particular, senescent vascular smooth muscle cells (VSMCs) have been observed within atherosclerotic plaques. Oxidants are widely implicated in vascular ageing and cardiovascular disease with evidence of oxidative stress in cells undergoing senescence. Our previous data showed that Angiotensin II caused stress induced premature senescence (SIPS) in primary human VSMC via oxidant generation. Prevention of senescence with a mitochondria targeted antioxidant, Mito-TEMPO, suggested the mechanism was dependent on mitochondria
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Rogers, Kara Emilie. "Mitochondrial Antioxidants, Protection Against Oxidative Stress, and the Role of Mitochondria in the Production of Reactive Oxygen Species." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194490.

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Mitochondria serve as the major source of reactive oxygen species (ROS) production in cells resulting in antioxidant systems and cell signaling pathways that are unique to mitochondria. Thioredoxin-2 (Trx-2) is the mitochondrial member of the thioredoxin superfamily, and acts specifically to reduce the mitochondrial peroxidase, peroxiredoxin-3. It has been proposed that Trx-2 associates with cytochrome c, which functions in mitochondrial respiration and apoptosis. Homozygous Trx-2 deletion in mice is embryonic lethal and it is hypothesized here that Trx-2 lethality is caused by loss of mito
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Schwarzlander, Markus. "The Response to Mitochondrial Reactive Oxygen Species and Redox Status in Plants." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504582.

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

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Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa, ADT and Garlid, KD. Am J Physiol 295, H874-82, 2008). Superoxide (O2•-), hydrogen peroxide (H2O2), and hydroxyl radical (HO•) have each been proposed as the signaling ROS but the identity of the ROS responsi
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Hansson, Anna. "Cellular responses to respiratory chain dysfunction /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-493-7/.

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Książki na temat "Mitochondrial reactive oxygen species"

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service), ScienceDirect (Online, ed. Mitochondrial function: Mitochondrial electron transport complexes and reactive oxygen species. Amsterdam: Academic Press/Elsevier, 2009.

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Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.

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

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Espada, Jesús, ed. 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, and Antonio Cuadrado, eds. Reactive Oxygen Species. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68510-2.

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

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Rio, Luis Alfonso, and Alain Puppo, eds. 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., and 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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Smirnoff, Nicholas, ed. Antioxidants and Reactive Oxygen Species in Plants. Oxford, UK: Blackwell Publishing Ltd, 2005. http://dx.doi.org/10.1002/9780470988565.

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Części książek na temat "Mitochondrial reactive oxygen species"

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Papa, S., and V. P. Skulachev. "Reactive oxygen species, mitochondria, apoptosis and aging." In Detection of Mitochondrial Diseases, 305–19. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_47.

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Skulachev, V. P., and K. G. Lyamzaev. "Mitochondrial Reactive Oxygen Species Aging Theory." In Encyclopedia of Gerontology and Population Aging, 1–8. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_47-1.

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Nacarelli, Timothy, Claudio Torres, and Christian Sell. "Mitochondrial Reactive Oxygen Species in Cellular Senescence." In Cellular Ageing and Replicative Senescence, 169–85. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26239-0_10.

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Kembro, Jackelyn Melissa, Sonia Cortassa, and Miguel A. Aon. "Mitochondrial Reactive Oxygen Species (ROS) and Arrhythmias." In Systems Biology of Free Radicals and Antioxidants, 1047–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_69.

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Starkov, Anatoly A. "Measuring Mitochondrial Reactive Oxygen Species (ROS) Production." In Systems Biology of Free Radicals and Antioxidants, 265–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_8.

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Boehme, Jason, and Emin Maltepe. "Cellular Oxygen Sensing, Mitochondrial Oxygen Sensing and Reactive Oxygen Species." In Hypoxic Respiratory Failure in the Newborn, 96–100. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780367494018-17.

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Dakubo, Gabriel D. "The Role of Mitochondrial Reactive Oxygen Species in Cancer." In Mitochondrial Genetics and Cancer, 237–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11416-8_10.

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Delcambre, Sylvie, Yannic Nonnenmacher, and Karsten Hiller. "Dopamine Metabolism and Reactive Oxygen Species Production." In Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease, 25–47. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42139-1_2.

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Turrens, Julio F. "Formation of Reactive Oxygen Species in Mitochondria." In Mitochondria, 185–96. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-69945-5_8.

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Genova, Maria Luisa, Milena Merlo Pich, Andrea Bernacchia, Cristina Bianchi, Annalisa Biondi, Carla Bovina, Anna Ida Falasca, Gabriella Formiggini, Giovanna Parenti Castelli, and Giorgio Lenaz. "The Mitochondrial Production of Reactive Oxygen Species in Relation to Aging and Pathology." In Mitochondrial Pathogenesis, 86–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_10.

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Streszczenia konferencji na temat "Mitochondrial reactive oxygen species"

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Waliszewski, Przemyslaw, and 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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Belchamber, Kylie, Richa Singh, Jadwiga Wedzicha, Peter Barnes, and Louise Donnelly. "Elevated mitochondrial reactive oxygen species in COPD macrophages at exacerbation." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa387.

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ZOROV, DMITRY. "NONPHOSPHORYLATING OXIDATION IN MITOCHONDRIA AND PROBLEMS ASSOCIATED WITH MITOCHONDRIAL GENERATION OF REACTIVE OXYGEN SPECIES." In HOMO SAPIENS LIBERATUS. TORUS PRESS, 2020. http://dx.doi.org/10.30826/homosapiens-2020-01.

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Wang, Yongxing, Vikram Kulkarni, Jezzreel Pantaleon Garcia, Michael Longmire, Shradha Wali, and Scott Evans. "Phosphorothiorate oligodeoxynucleotides induce antimicrobial epithelial mitochondrial reactive oxygen species that protect against pneumonia." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2331.

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Pak, Oleg, Natascha Sommer, Thomas Derfuss, Alfons Krug, Erich Gnaiger, HosseinA Ghofrani, Ralph T. Schermuly, Werner Seeger, Friedrich Grimminger, and Norbert Weissmann. "Mitochondrial Respiration And Reactive Oxygen Species In Acute Pulmonary Oxygen Sensing Of Pulmonary Arterial Smooth Muscle Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3937.

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Fedyaeva, A. V., I. V. Lyubushkina, A. V. Stepanov, Y. Li, A. V. Sidorov, and E. G. Rikhvanov. "MITOCHONDRIAL MEMBRANE POTENTIAL AND REACTIVE OXYGEN SPECIES, AS INDICATORS OF STRESS STATUS OF PLANTS." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-781-785.

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Michaeloudes, Charalambos, Paul Kirkham, Ian M. Adcock, and Kian Fan Chung. "Mitochondrial reactive oxygen species and glycolysis in airway smooth muscle cell proliferation in COPD." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa488.

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Malhotra, Anshu, Abhinav Dey, and Anna M. Kenney. "Abstract 2411: Reactive Oxygen Species regulates tumor stem cell survival in medulloblastoma via mitochondrial biogenesis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2411.

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Xu, Bingling, Serkan Cakir, Christian Badhan, Christopher Hui, Kian Fan Chung, and Pankaj Bhavsar. "Altered mitochondrial reactive oxygen species (ROS) production in airway smooth muscle cells of severe asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5204.

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Kim, Young Sam, Seon-Jin Lee, Hong Pyo Kim, and Augustine M. K. Choi. "Carbon Monoxide Induces Autophagy In Respiratory Epithelial Cells By Generation Of Mitochondrial Reactive Oxygen Species." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4177.

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Raporty organizacyjne na temat "Mitochondrial 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, April 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, April 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, January 2000. http://dx.doi.org/10.15760/etd.1640.

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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, July 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, July 2003. http://dx.doi.org/10.21236/ada418669.

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

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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, June 2018. http://dx.doi.org/10.31487/j.dobcr.2018.02.005.

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Hase, Travis. In Vivo Quantification of Reactive Oxygen Species Demonstrates High Levels of Oxidative Stress in Base Excision Repair-Deficient Caenorhabditis Elegans: Implications for Associative Metabolic Phenotypes. Portland State University Library, January 2013. http://dx.doi.org/10.15760/honors.10.

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