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Artykuły w czasopismach na temat „Mitochondrial reactive oxygen species”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 19 lutego 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Venditti, Paola, Lisa Di Stefano, and Sergio Di Meo. "Mitochondrial metabolism of reactive oxygen species." Mitochondrion 13, no. 2 (March 2013): 71–82. http://dx.doi.org/10.1016/j.mito.2013.01.008.

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12

Turrens, J. F. "Mitochondrial formation of reactive oxygen species." Journal of Physiology 552, no. 2 (October 15, 2003): 335–44. http://dx.doi.org/10.1113/jphysiol.2003.049478.

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13

Grivennikova, V. G., and A. D. Vinogradov. "Mitochondrial production of reactive oxygen species." Biochemistry (Moscow) 78, no. 13 (December 2013): 1490–511. http://dx.doi.org/10.1134/s0006297913130087.

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14

Andreyev, A. Yu, Yu E. Kushnareva, and A. A. Starkov. "Mitochondrial metabolism of reactive oxygen species." Biochemistry (Moscow) 70, no. 2 (February 2005): 200–214. http://dx.doi.org/10.1007/s10541-005-0102-7.

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15

Kirkinezos, Ilias G., and Carlos T. Moraes. "Reactive oxygen species and mitochondrial diseases." Seminars in Cell & Developmental Biology 12, no. 6 (December 2001): 449–57. http://dx.doi.org/10.1006/scdb.2001.0282.

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16

Zimmerman, Matthew C., and Irving H. Zucker. "Mitochondrial Dysfunction and Mitochondrial-Produced Reactive Oxygen Species." Hypertension 53, no. 2 (February 2009): 112–14. http://dx.doi.org/10.1161/hypertensionaha.108.125567.

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17

Kong, Hyewon, Colleen R. Reczek, Gregory S. McElroy, Elizabeth M. Steinert, Tim Wang, David M. Sabatini, and Navdeep S. Chandel. "Metabolic determinants of cellular fitness dependent on mitochondrial reactive oxygen species." Science Advances 6, no. 45 (November 2020): eabb7272. http://dx.doi.org/10.1126/sciadv.abb7272.

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Mitochondria-derived reactive oxygen species (mROS) are required for the survival, proliferation, and metastasis of cancer cells. The mechanism by which mitochondrial metabolism regulates mROS levels to support cancer cells is not fully understood. To address this, we conducted a metabolism-focused CRISPR-Cas9 genetic screen and uncovered that loss of genes encoding subunits of mitochondrial complex I was deleterious in the presence of the mitochondria-targeted antioxidant mito-vitamin E (MVE). Genetic or pharmacologic inhibition of mitochondrial complex I in combination with the mitochondria-

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18

Chan, Samuel H. H., and Julie Y. H. Chan. "Mitochondria and Reactive Oxygen Species Contribute to Neurogenic Hypertension." Physiology 32, no. 4 (July 2017): 308–21. http://dx.doi.org/10.1152/physiol.00006.2017.

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Beyond its primary role as fuel generators, mitochondria are engaged in a variety of cellular processes, including redox homeostasis. Mitochondrial dysfunction, therefore, may have a profound impact on high-energy-demanding organs such as the brain. Here, we review the roles of mitochondrial biogenesis and bioenergetics, and their associated signaling in cellular redox homeostasis, and illustrate their contributions to the oxidative stress-related neural mechanism of hypertension, focusing on specific brain areas that are involved in the generation or modulation of sympathetic outflows to the

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19

Nohl, Hans, Lars Gille, and Katrin Staniek. "The mystery of reactive oxygen species derived from cell respiration." Acta Biochimica Polonica 51, no. 1 (March 31, 2004): 223–29. http://dx.doi.org/10.18388/abp.2004_3615.

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Mitochondrial respiration is considered to provide reactive oxygen species (ROS) as byproduct of regular electron transfer. Objections were raised since results obtained with isolated mitochondria are commonly transferred to activities of mitochondria in the living cell. High electrogenic membrane potential was reported to trigger formation of mitochondrial ROS involving complex I and III. Suggested bioenergetic parameters, starting ROS formation, widely change with the isolation mode. ROS detection systems generally applied may be misleading due to possible interactions with membrane constitu

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20

Hoffman, David L., and Paul S. Brookes. "Oxygen Sensitivity of Mitochondrial Reactive Oxygen Species Generation Depends on Metabolic Conditions." Journal of Biological Chemistry 284, no. 24 (April 14, 2009): 16236–45. http://dx.doi.org/10.1074/jbc.m809512200.

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The mitochondrial generation of reactive oxygen species (ROS) plays a central role in many cell signaling pathways, but debate still surrounds its regulation by factors, such as substrate availability, [O2] and metabolic state. Previously, we showed that in isolated mitochondria respiring on succinate, ROS generation was a hyperbolic function of [O2]. In the current study, we used a wide variety of substrates and inhibitors to probe the O2 sensitivity of mitochondrial ROS generation under different metabolic conditions. From such data, the apparent Km for O2 of putative ROS-generating sites wi

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21

Hernansanz-Agustín, Pablo, and José Antonio Enríquez. "Generation of Reactive Oxygen Species by Mitochondria." Antioxidants 10, no. 3 (March 9, 2021): 415. http://dx.doi.org/10.3390/antiox10030415.

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Reactive oxygen species (ROS) are series of chemical products originated from one or several electron reductions of oxygen. ROS are involved in physiology and disease and can also be both cause and consequence of many biological scenarios. Mitochondria are the main source of ROS in the cell and, particularly, the enzymes in the electron transport chain are the major contributors to this phenomenon. Here, we comprehensively review the modes by which ROS are produced by mitochondria at a molecular level of detail, discuss recent advances in the field involving signalling and disease, and the inv

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22

von Bergen, Nicholas H., Stacia L. Koppenhafer, Douglas R. Spitz, Kenneth A. Volk, Sonali S. Patel, Robert D. Roghair, Fred S. Lamb, Jeffrey L. Segar, and Thomas D. Scholz. "Fetal programming alters reactive oxygen species production in sheep cardiac mitochondria." Clinical Science 116, no. 8 (March 16, 2009): 659–68. http://dx.doi.org/10.1042/cs20080474.

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Exposure to an adverse intrauterine environment is recognized as an important risk factor for the development of cardiovascular disease later in life. Although oxidative stress has been proposed as a mechanism for the fetal programming phenotype, the role of mitochondrial O2•− (superoxide radical) production has not been explored. To determine whether mitochondrial ROS (reactive oxygen species) production is altered by in utero programming, pregnant ewes were given a 48-h dexamethasone (dexamethasone-exposed, 0.28 mg·kg−1 of body weight·day−1) or saline (control) infusion at 27–28 days gestati

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23

Garlid, Anders O., Martin Jaburek, Jeremy P. Jacobs, and Keith D. Garlid. "Mitochondrial reactive oxygen species: which ROS signals cardioprotection?" American Journal of Physiology-Heart and Circulatory Physiology 305, no. 7 (October 1, 2013): H960—H968. http://dx.doi.org/10.1152/ajpheart.00858.2012.

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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 AD, Garlid KD. Am J Physiol Heart Circ Physiol 295, H874–H882, 2008). The ROS responsible for this effect is not known. The present study focuses on superoxide (O2·−), hydrogen peroxide (H2O2), and hydroxyl r

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24

Yang, Zhi-wei, and Fu-yu Yang. "Sensitivity of Ca2+ Transport of Mitochondria to Reactive Oxygen Species." Bioscience Reports 17, no. 6 (December 1, 1997): 557–67. http://dx.doi.org/10.1023/a:1027316424985.

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The relationship between Ca2+ transport and energy transduction of myocardial mitochondria in the presence of reactive oxygen species was investigated. Following treatment with oxygen free radicals [superoxide(O2•) or hydroxyl radical (•)OH], lipid free radicals in myocardial mitochondrial membrane could be detected by using the method of EPR spin trap. Simultaneously there were obvious alterations in the free Ca2+ ([Ca2+]m) in the mitochondrial matrix; the physical state of membrane lipid; the efficiency of oxidative phosphorylation (ADP/O); the value of the respiratory control ratio (RCR); a

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25

Quarrie, Ricardo, Daniel S. Lee, Levy Reyes, Warren Erdahl, Douglas R. Pfeiffer, Jay L. Zweier, and Juan A. Crestanello. "Mitochondrial uncoupling does not decrease reactive oxygen species production after ischemia-reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 7 (October 1, 2014): H996—H1004. http://dx.doi.org/10.1152/ajpheart.00189.2014.

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Cardiac ischemia-reperfusion (IR) leads to myocardial dysfunction by increasing production of reactive oxygen species (ROS). Mitochondrial H+ leak decreases ROS formation; it has been postulated that increasing H+ leak may be a mechanism of decreasing ROS production after IR. Ischemic preconditioning (IPC) decreases ROS formation after IR, but the mechanism is unknown. We hypothesize that pharmacologically increasing mitochondrial H+ leak would decrease ROS production after IR. We further hypothesize that IPC would be associated with an increase in the rate of H+ leak. Isolated male Sprague-Da

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26

Sena, Laura A., and Navdeep S. Chandel. "Physiological Roles of Mitochondrial Reactive Oxygen Species." Molecular Cell 48, no. 2 (October 2012): 158–67. http://dx.doi.org/10.1016/j.molcel.2012.09.025.

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27

Ito, Hiromu, and Hirofumi Matsui. "Mitochondrial Reactive Oxygen Species and Photodynamic Therapy." LASER THERAPY 25, no. 3 (2016): 193–99. http://dx.doi.org/10.5978/islsm.16-or-15.

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Nickel, Alexander, Michael Kohlhaas, and Christoph Maack. "Mitochondrial reactive oxygen species production and elimination." Journal of Molecular and Cellular Cardiology 73 (August 2014): 26–33. http://dx.doi.org/10.1016/j.yjmcc.2014.03.011.

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29

Freed, Julie K., and David D. Gutterman. "Mitochondrial Reactive Oxygen Species and Vascular Function." Arteriosclerosis, Thrombosis, and Vascular Biology 33, no. 4 (April 2013): 673–75. http://dx.doi.org/10.1161/atvbaha.13.301039.

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Oliveira, Graciele A., and Alicia J. Kowaltowski. "Phosphate Increases Mitochondrial Reactive Oxygen Species Release." Free Radical Research 38, no. 10 (October 2004): 1113–18. http://dx.doi.org/10.1080/10715760400009258.

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Levin, Leonard A. "Reactive Oxygen Species in Mitochondrial Optic Neuropathies." Journal of Neuro-Ophthalmology 35, no. 4 (December 2015): 446. http://dx.doi.org/10.1097/wno.0000000000000323.

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Sadun, Alfredo A., Rustum Karanjia, Billy X. Pan, Fred N. Ross-Cisneros, and Valerio Carelli. "Reactive Oxygen Species in Mitochondrial Optic Neuropathies." Journal of Neuro-Ophthalmology 35, no. 4 (December 2015): 445–46. http://dx.doi.org/10.1097/wno.0000000000000324.

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33

Debattisti, Valentina, Masao Saotome, Sudipto Das, and Gyorgy Hajnoczky. "Reactive Oxygen Species (ROS) Suppress Mitochondrial Motility." Biophysical Journal 108, no. 2 (January 2015): 610a. http://dx.doi.org/10.1016/j.bpj.2014.11.3320.

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Hamanaka, Robert B., and Navdeep S. Chandel. "Mitochondrial reactive oxygen species regulate hypoxic signaling." Current Opinion in Cell Biology 21, no. 6 (December 2009): 894–99. http://dx.doi.org/10.1016/j.ceb.2009.08.005.

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Malinska, Dominika, Sandra R. Mirandola, and Wolfram S. Kunz. "Mitochondrial potassium channels and reactive oxygen species." FEBS Letters 584, no. 10 (January 16, 2010): 2043–48. http://dx.doi.org/10.1016/j.febslet.2010.01.013.

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Rogov, Anton G., Tatiana N. Goleva, Khoren K. Epremyan, Igor I. Kireev, and Renata A. Zvyagilskaya. "Propagation of Mitochondria-Derived Reactive Oxygen Species within the Dipodascus magnusii Cells." Antioxidants 10, no. 1 (January 15, 2021): 120. http://dx.doi.org/10.3390/antiox10010120.

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Mitochondria are considered to be the main source of reactive oxygen species (ROS) in the cell. It was shown that in cardiac myocytes exposed to excessive oxidative stress, ROS-induced ROS release is triggered. However, cardiac myocytes have a network of densely packed organelles that do not move, which is not typical for the majority of eukaryotic cells. The purpose of this study was to trace the spatiotemporal development (propagation) of prooxidant-induced oxidative stress and its interplay with mitochondrial dynamics. We used Dipodascus magnusii yeast cells as a model, as they have advanta

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37

Jankó, Laura, Tünde Kovács, Miklós Laczik, Zsanett Sári, Gyula Ujlaki, Gréta Kis, Ibolya Horváth, et al. "Silencing of Poly(ADP-Ribose) Polymerase-2 Induces Mitochondrial Reactive Species Production and Mitochondrial Fragmentation." Cells 10, no. 6 (June 4, 2021): 1387. http://dx.doi.org/10.3390/cells10061387.

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PARP2 is a DNA repair protein. The deletion of PARP2 induces mitochondrial biogenesis and mitochondrial activity by increasing NAD+ levels and inducing SIRT1 activity. We show that the silencing of PARP2 causes mitochondrial fragmentation in myoblasts. We assessed multiple pathways that can lead to mitochondrial fragmentation and ruled out the involvement of mitophagy, the fusion–fission machinery, SIRT1, and mitochondrial unfolded protein response. Nevertheless, mitochondrial fragmentation was reversed by treatment with strong reductants, such as reduced glutathione (GSH), N-acetyl-cysteine (

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38

Kausar, Saima, Feng Wang, and Hongjuan Cui. "The Role of Mitochondria in Reactive Oxygen Species Generation and Its Implications for Neurodegenerative Diseases." Cells 7, no. 12 (December 17, 2018): 274. http://dx.doi.org/10.3390/cells7120274.

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Mitochondria are dynamic cellular organelles that consistently migrate, fuse, and divide to modulate their number, size, and shape. In addition, they produce ATP, reactive oxygen species, and also have a biological role in antioxidant activities and Ca2+ buffering. Mitochondria are thought to play a crucial biological role in most neurodegenerative disorders. Neurons, being high-energy-demanding cells, are closely related to the maintenance, dynamics, and functions of mitochondria. Thus, impairment of mitochondrial activities is associated with neurodegenerative diseases, pointing to the signi

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Dikalov, Sergey I., Wei Li, Abdulrahman K. Doughan, Raul R. Blanco, and A. Maziar Zafari. "Mitochondrial reactive oxygen species and calcium uptake regulate activation of phagocytic NADPH oxidase." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 10 (May 15, 2012): R1134—R1142. http://dx.doi.org/10.1152/ajpregu.00842.2010.

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Production of superoxide (O2·−) by NADPH oxidases contributes to the development of hypertension and atherosclerosis. Factors responsible for activation of NADPH oxidases are not well understood; interestingly, cardiovascular disease is associated with both altered NADPH oxidase activity and age-associated mitochondrial dysfunction. We hypothesized that mitochondrial dysfunction may contribute to activation of NADPH oxidase. The effect of mitochondrial inhibitors on phagocytic NADPH oxidase in human lymphoblasts and whole blood was measured at the basal state and upon PKC-dependent stimulation

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40

SEDENSKY, M., and P. GMORGAN. "Mitochondrial respiration and reactive oxygen species in mitochondrial aging mutants." Experimental Gerontology 41, no. 3 (March 2006): 237–45. http://dx.doi.org/10.1016/j.exger.2006.01.004.

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KAGEYAMA, Mio, Jun ITO, Koumei SHIRASUNA, Takehito KUWAYAMA, and Hisataka IWATA. "Mitochondrial reactive oxygen species regulate mitochondrial biogenesis in porcine embryos." Journal of Reproduction and Development 67, no. 2 (2021): 141–47. http://dx.doi.org/10.1262/jrd.2020-111.

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42

Hoffman, David L., Jason D. Salter, and Paul S. Brookes. "Response of mitochondrial reactive oxygen species generation to steady-state oxygen tension: implications for hypoxic cell signaling." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H101—H108. http://dx.doi.org/10.1152/ajpheart.00699.2006.

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Mitochondria are proposed to play an important role in hypoxic cell signaling. One currently accepted signaling paradigm is that the mitochondrial generation of reactive oxygen species (ROS) increases in hypoxia. This is paradoxical, because oxygen is a substrate for ROS generation. Although the response of isolated mitochondrial ROS generation to [O2] has been examined previously, such investigations did not apply rigorous control over [O2] within the hypoxic signaling range. With the use of open-flow respirometry and fluorimetry, the current study determined the response of isolated rat live

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Poirault-Chassac, Sonia, Valérie Nivet-Antoine, Amandine Houvert, Alexandre Kauskot, Evelyne Lauret, René Lai-Kuen, Isabelle Dusanter-Fourt, and Dominique Baruch. "Mitochondrial dynamics and reactive oxygen species initiate thrombopoiesis from mature megakaryocytes." Blood Advances 5, no. 6 (March 15, 2021): 1706–18. http://dx.doi.org/10.1182/bloodadvances.2020002847.

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Abstract Blood platelets are essential for controlling hemostasis. They are released by megakaryocytes (MKs) located in the bone marrow, upon extension of cytoplasmic protrusions into the lumen of bone marrow sinusoids. Their number increases in postpulmonary capillaries, suggesting a role for oxygen gradient in thrombopoiesis (ie, platelet biogenesis). In this study, we show that initiation of thrombopoiesis from human mature MKs was enhanced under hyperoxia or during pro-oxidant treatments, whereas antioxidants dampened it. Quenching mitochondrial reactive oxygen species (mtROS) with MitoTEM

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Tauffenberger, Arnaud, and Pierre J. Magistretti. "Reactive Oxygen Species: Beyond Their Reactive Behavior." Neurochemical Research 46, no. 1 (January 2021): 77–87. http://dx.doi.org/10.1007/s11064-020-03208-7.

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AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more com

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Al-Gubory, Kaïs H. "Mitochondria: Omega-3 in the route of mitochondrial reactive oxygen species." International Journal of Biochemistry & Cell Biology 44, no. 9 (September 2012): 1569–73. http://dx.doi.org/10.1016/j.biocel.2012.06.003.

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Teixeira, José, Cláudia M. Deus, Fernanda Borges, and Paulo J. Oliveira. "Mitochondria: Targeting mitochondrial reactive oxygen species with mitochondriotropic polyphenolic-based antioxidants." International Journal of Biochemistry & Cell Biology 97 (April 2018): 98–103. http://dx.doi.org/10.1016/j.biocel.2018.02.007.

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Hoeft, Konrad, Donald B. Bloch, Jan A. Graw, Rajeev Malhotra, Fumito Ichinose, and Aranya Bagchi. "Iron Loading Exaggerates the Inflammatory Response to the Toll-like Receptor 4 Ligand Lipopolysaccharide by Altering Mitochondrial Homeostasis." Anesthesiology 127, no. 1 (July 1, 2017): 121–35. http://dx.doi.org/10.1097/aln.0000000000001653.

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Abstract Background Perioperative and critically ill patients are often exposed to iron (in the form of parenteral-iron administration or blood transfusion) and inflammatory stimuli, but the effects of iron loading on the inflammatory response are unclear. Recent data suggest that mitochondrial reactive oxygen species have an important role in the innate immune response and that increased mitochondrial reactive oxygen species production is a result of dysfunctional mitochondria. We tested the hypothesis that increased intracellular iron potentiates lipopolysaccharide-induced inflammation by in

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Pecinova, Alena, Zdenek Drahota, Jana Kovalcikova, Nikola Kovarova, Petr Pecina, Lukas Alan, Michal Zima, Josef Houstek, and Tomas Mracek. "Pleiotropic Effects of Biguanides on Mitochondrial Reactive Oxygen Species Production." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/7038603.

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Metformin is widely prescribed as a first-choice antihyperglycemic drug for treatment of type 2 diabetes mellitus, and recent epidemiological studies showed its utility also in cancer therapy. Although it is in use since the 1970s, its molecular target, either for antihyperglycemic or antineoplastic action, remains elusive. However, the body of the research on metformin effect oscillates around mitochondrial metabolism, including the function of oxidative phosphorylation (OXPHOS) apparatus. In this study, we focused on direct inhibitory mechanism of biguanides (metformin and phenformin) on OXP

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Cortassa, Sonia, Miguel A. Aon, Raimond L. Winslow, and Brian O’Rourke. "A Mitochondrial Oscillator Dependent on Reactive Oxygen Species." Biophysical Journal 87, no. 3 (September 2004): 2060–73. http://dx.doi.org/10.1529/biophysj.104.041749.

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MA, Qi, Lei LIU, and Quan CHEN. "Reactive Oxygen Species, Mitochondrial Permeability Transition and Apoptosis." ACTA BIOPHYSICA SINICA 28, no. 7 (2012): 523. http://dx.doi.org/10.3724/sp.j.1260.2012.20103.

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