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Journal articles on the topic 'Mitochondrial reactive oxygen species'

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Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 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 modes of operation by isolated mitochondria result in significant O2•− production, predominantly from complex I: (i) when the mitochondria are not making ATP and consequently have a high Δp (protonmotive force) and a reduced CoQ (coenzyme Q) pool; and (ii) when there is a high NADH/NAD+ ratio in the mitochondrial matrix. For mitochondria that are actively making ATP, and consequently have a lower Δp and NADH/NAD+ ratio, the extent of O2•− production is far lower. The generation of O2•− within the mitochondrial matrix depends critically on Δp, the NADH/NAD+ and CoQH2/CoQ ratios and the local O2 concentration, which are all highly variable and difficult to measure in vivo. Consequently, it is not possible to estimate O2•− generation by mitochondria in vivo from O2•−-production rates by isolated mitochondria, and such extrapolations in the literature are misleading. Even so, the description outlined here facilitates the understanding of factors that favour mitochondrial ROS production. There is a clear need to develop better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

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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. This regenerative cycle of mitochondrial ROS formation and release was named ROS-induced ROS release (RIRR). Brief, reversible mPTP opening-associated ROS release apparently constitutes an adaptive housekeeping function by the timely release from mitochondria of accumulated potentially toxic levels of ROS (and Ca2+). At higher ROS levels, longer mPTP openings may release a ROS burst leading to destruction of mitochondria, and if propagated from mitochondrion to mitochondrion, of the cell itself. The destructive function of RIRR may serve a physiological role by removal of unwanted cells or damaged mitochondria, or cause the pathological elimination of vital and essential mitochondria and cells. The adaptive release of sufficient ROS into the vicinity of mitochondria may also activate local pools of redox-sensitive enzymes involved in protective signaling pathways that limit ischemic damage to mitochondria and cells in that area. Maladaptive mPTP- or IMAC-related RIRR may also be playing a role in aging. Because the mechanism of mitochondrial RIRR highlights the central role of mitochondria-formed ROS, we discuss all of the known ROS-producing sites (shown in vitro) and their relevance to the mitochondrial ROS production in vivo.

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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 depolarization. This phenomenon was ascribed to MPT induction because (a) bongkrekic acid prevented it and (b) mitochondria became permeable for calcein (∼620 daltons) concurrently with depolarization. These photodynamically produced “triggering” ROS caused the MPT induction, as the ROS scavenger Trolox prevented it. The time required for triggering ROS to induce the MPT was dependent on intrinsic cellular ROS-scavenging redox mechanisms, particularly glutathione. MPT induction caused by triggering ROS coincided with a burst of mitochondrial ROS generation, as measured by dichlorofluorescein fluorescence, which we have termed mitochondrial “ROS-induced ROS release” (RIRR). This MPT induction/RIRR phenomenon in cardiac myocytes often occurred synchronously and reversibly among long chains of adjacent mitochondria demonstrating apparent cooperativity. The observed link between MPT and RIRR could be a fundamental phenomenon in mitochondrial and cell biology.

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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. Several Ca2+ transport systems are modulated by oxidation. Oxidation increases the activity of inositol 1,4,5-trisphosphate and ryanodine receptors, the main channels releasing Ca2+ from intracellular stores in response to cellular stimulation. On the other hand, mitochondria are known to control [Ca2+]i signals by Ca2+ uptake and release during cytosolic calcium mobilization, specially in mitochondria situated close to Ca2+ release channels. Mitochondrial inhibitors modify calcium signals in numerous cell types, including oscillations evoked by physiological stimulus. Although these inhibitors reduce mitochondrial Ca2+ uptake, they also impair ROS production in several systems. In keeping with this effect, recent reports show that antioxidants or oxidant scavengers also inhibit physiological calcium signals. Furthermore, there is evidence that mitochondria generate ROS in response to cell stimulation, an effect suppressed by mitochondrial inhibitors that simultaneously block [Ca2+]i signals. Together, the data reviewed here indicate that Ca2+-mobilizing stimulus generates mitochondrial ROS, which, in turn, facilitate [Ca2+]i signals, a new aspect in the biology of mitochondria. Finally, the potential implications for biological modeling are discussed.

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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 involvement of the oxidative stress in the regulation of some actors of mitochondrial biogenesis.

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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 functions in mitochondria. This is exemplified by the control of mitochondrial and cellular calcium homeostasis, whose understanding has improved greatly during the last few years. An exciting new aspect is the discovery that nitric oxide and congeners have an enormous impact on mitochondria. Physiological concentrations of nitrogen monoxide (NO) at physiological cellular oxygen pressure inhibit cytochrome oxidase and thereby respiration. A transient inhibition of cytochrome oxidase by NO appears to be used in at least some forms of cell signalling. Peroxynitrite, the product of the reaction between superoxide and NO, can stimulate the specific calcium release pathway from mitochondria by oxidizing some vicinal thiols in mitochondria. There is evidence mounting that mitochondrial calcium handling and its modulation by reactive oxygen and nitrogen species is important for necrotic and apoptotic cell death.

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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 postulating that, in addition to producing ATP, mitochondria also play a key role in cell signaling and regulate a variety of cellular functions. This review focuses on the emerging role of mitochondrial ROS as signaling molecules in vascular endothelial cells. Specifically, we discuss some recent findings that indicate that mitochondrial ROS regulate vascular endothelial function, focusing on major sites of ROS production in endothelial mitochondria, factors modulating mitochondrial ROS production, the physiological and clinical implications of endothelial mitochondrial ROS, and methodological considerations in the study of mitochondrial contribution to vascular ROS generation.

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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 are enriched with H2O2 degrading enzymes to desensitize redox signals. These organelles also use a series of negative feedback loops, such as proton leaks or protein S-glutathionylation, to inhibit H2O2 production. Understanding how mitochondria produce ROS is also important for comprehending how these organelles use H2O2 in eustress signaling. Indeed, twelve different enzymes associated with nutrient metabolism and oxidative phosphorylation (OXPHOS) can serve as important ROS sources. This includes several flavoproteins and respiratory complexes I-III. Progress in understanding how mitochondria generate H2O2 for signaling must also account for critical physiological factors that strongly influence ROS production, such as sex differences and genetic variances in genes encoding antioxidants and proteins involved in mitochondrial bioenergetics. In the present review, I provide an updated view on how mitochondria budget cellular H2O2 production. These discussions will focus on the potential addition of two acyl-CoA dehydrogenases to the list of ROS generators and the impact of important phenotypic and physiological factors such as tissue type, mouse strain, and sex on production by these individual sites.

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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. To test these hypotheses, we examined H2O2generation by diaphragm mitochondria isolated from saline-treated control and endotoxin-treated septic animals in the presence and absence of calcium and ADP; we also assessed the effect of PLA2inhibitors on H2O2formation. We found that 1) calcium and ADP stimulated H2O2formation by diaphragm mitochondria from both control and septic animals; 2) mitochondria from septic animals demonstrated substantially higher H2O2formation than mitochondria from control animals under basal, calcium-stimulated, and ADP-stimulated conditions; and 3) inhibitors of 14-kDa PLA2blocked the enhanced H2O2generation in all conditions. We also found that administration of arachidonic acid (the principal metabolic product of PLA2activation) increased mitochondrial H2O2formation by interacting with complex I of the electron transport chain. These data suggest that diaphragm mitochondrial ROS formation during contraction and sepsis may be critically dependent on PLA2activation.

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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-targeted antioxidants, MVE or MitoTEMPO, induced a robust integrated stress response (ISR) and markedly diminished cell survival and proliferation in vitro. This was not observed following inhibition of mitochondrial complex III. Administration of MitoTEMPO in combination with the mitochondrial complex I inhibitor phenformin decreased the leukemic burden in a mouse model of T cell acute lymphoblastic leukemia. Thus, mitochondrial complex I is a dominant metabolic determinant of mROS-dependent cellular fitness.

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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 cardiovascular system. We also highlight future challenges of research on mitochondrial physiology and pathophysiology.

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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 constituents or electron carriers. Avoiding these problems no conditions reported to transform mitochondrial respiration to a radical source were confirmed. However, changing the physical membrane state affected the highly susceptible interaction of the ubiquinol/bc(1) redox complex such that ROS formation became possible.

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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 within mitochondria was estimated as follows: 0.2, 0.9, 2.0, and 5.0 μm O2 for the complex I flavin site, complex I electron backflow, complex III QO site, and electron transfer flavoprotein quinone oxidoreductase of β-oxidation, respectively. Differential effects of respiratory inhibitors on ROS generation were also observed at varying [O2]. Based on these data, we hypothesize that at physiological [O2], complex I is a significant source of ROS, whereas the electron transfer flavoprotein quinone oxidoreductase may only contribute to ROS generation at very high [O2]. Furthermore, we suggest that previous discrepancies in the assignment of effects of inhibitors on ROS may be due to differences in experimental [O2]. Finally, the data set (see supplemental material) may be useful in the mathematical modeling of mitochondrial metabolism.

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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 involvement of supercomplexes in these mechanisms. Given the importance of mitochondrial ROS, we also provide a schematic guide aimed to help in deciphering the mechanisms involved in their production in a variety of physiological and pathological settings.

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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 gestation (term=145 days). Intact left ventricular mitochondria and freeze-thaw mitochondrial membranes were studied from offspring at 4-months of age. AmplexRed was used to measure H2O2 production. Activities of the antioxidant enzymes Mn-SOD (manganese superoxide dismutase), GPx (glutathione peroxidase) and catalase were measured. Compared with controls, a significant increase in Complex I H2O2 production was found in intact mitochondria from dexamethasone-exposed animals. The treatment differences in Complex I-driven H2O2 production were not seen in mitochondrial membranes. Consistent changes in H2O2 production from Complex III in programmed animals were not found. Despite the increase in H2O2 production in intact mitochondria from programmed animals, dexamethasone exposure significantly increased mitochondrial catalase activity, whereas Mn-SOD and GPx activities were unchanged. The results of the present study point to an increase in the rate of release of H2O2 from programmed mitochondria despite an increase in catalase activity. Greater mitochondrial H2O2 release into the cell may play a role in the development of adult disease following exposure to an adverse intrauterine environment.

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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 radical (HO˙), each of which has been proposed as the signaling ROS. Feedback activation of mitoKATP provides an ideal setting for studying endogenous ROS signaling. Respiring rat heart mitochondria were preincubated with ATP and diazoxide, together with an agent being tested for interference with this process, either by scavenging ROS or by blocking ROS transformations. The mitochondria were then assayed to determine whether or not the persistent phosphorylated open state was achieved. Dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, Trolox, and bromoenol lactone each interfered with formation of the ROS-dependent open state. Catalase did not interfere with this step. We also found that DMF blocked cardioprotection by both ischemic preconditioning and diazoxide. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO˙ excludes H2O2 as the endogenous signaling ROS. Taken together, the results support the conclusion that the ROS message is carried by a downstream product of HO˙ and that it is probably a product of phospholipid oxidation.

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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); and the membrane potential of the inner membrane of myocardial mitochondria. If the concentrations of reactive oxygen species were reduced by about 30%, the alterations in the physical state of the membrane lipid and energy transduction of myocardial mitochondria were not observed, but the changes in Ca2+ homeostasis remained. We conclude that Ca2+ transport by myocardial mitochondria is more sensitive to agents such as (O2•) or •OH, etc. than are oxidation phosphorylation and the respiratory chain.

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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-Dawley rat hearts were subjected to either control or IPC. Mitochondria were isolated at end equilibration, end ischemia, and end reperfusion. Mitochondrial membrane potential (mΔΨ) was measured using a tetraphenylphosphonium electrode. Mitochondrial uncoupling was achieved by adding increasing concentrations of FCCP. Mitochondrial ROS production was measured by fluorometry using Amplex-Red. Pyridine dinucleotide levels were measured using HPLC. Before IR, increasing H+ leak decreased mitochondrial ROS production. After IR, ROS production was not affected by increasing H+ leak. H+ leak increased at end ischemia in control mitochondria. IPC mitochondria showed no change in the rate of H+ leak throughout IR. NADPH levels decreased after IR in both IPC and control mitochondria while NADH increased. Pharmacologically, increasing H+ leak is not a method of decreasing ROS production after IR. Replenishing the NADPH pool may be a means of scavenging the excess ROS thereby attenuating oxidative damage after IR.

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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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28

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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30

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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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 advantages over other models, including a uniquely large size, mitochondria that are easy to visualize and freely moving, an ability to vigorously grow on well-defined low-cost substrates, and high responsibility. It was shown that prooxidant-induced oxidative stress was initiated in mitochondria, far preceding the appearance of generalized oxidative stress in the whole cell. For yeasts, these findings were obtained for the first time. Preincubation of yeast cells with SkQ1, a mitochondria-addressed antioxidant, substantially diminished production of mitochondrial ROS, while only slightly alleviating the generalized oxidative stress. This was expected, but had not yet been shown. Importantly, mitochondrial fragmentation was found to be primarily induced by mitochondrial ROS preceding the generalized oxidative stress development.

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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 (NAC), and a mitochondria-specific antioxidant MitoTEMPO. The effect of MitoTEMPO on mitochondrial morphology indicates the production of reactive oxygen species of mitochondrial origin. Elimination of reactive oxygen species reversed mitochondrial fragmentation in PARP2-silenced cells.

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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 significance of mitochondrial functions in normal cell physiology. In recent years, considerable progress has been made in our knowledge of mitochondrial functions, which has raised interest in defining the involvement of mitochondrial dysfunction in neurodegenerative diseases. Here, we summarize the existing knowledge of the mitochondrial function in reactive oxygen species generation and its involvement in the development of neurodegenerative diseases.

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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 with PMA using extracellular 1-hydroxy-2,2,6,6-tetramethylpiperidin-4-yl-trimethylammonium or mitochondria-targeted 1-hydroxy-4-[2-triphenylphosphonio)-acetamido]-2,2,6,6-tetramethylpiperidine spin probes and electron spin resonance (ESR). Intracellular cytosolic calcium [Ca2+]iwas measured spectrofluorometrically using fura-2 AM. Incubation of lymphoblasts with the mitochondrial inhibitors rotenone, antimycin A, CCCP, or ruthenium red (an inhibitor of mitochondrial Ca2+uniporter) did not significantly change basal activity of NADPH oxidase. In contrast, preincubation with the mitochondrial inhibitors prior to PMA stimulation of lymphoblasts resulted in two- to three-fold increase of NADPH oxidase activity compared with stimulation with PMA alone. Most notably, the intracellular Ca2+-chelating agent BAPTA-AM abolished the effect of mitochondrial inhibitors on NADPH oxidase activity. Cytosolic Ca2+measurements with fura-2 AM showed that the mitochondrial inhibitors increased [Ca2+]i, while BAPTA-AM abolished the increase in [Ca2+]i. Furthermore, depletion of cellular Ca2+with thapsigargin attenuated CCCP- and antimycin A-mediated activation of NADPH oxidase in the presence of PMA by 42% and 31%, correspondingly. Our data suggest that mitochondria regulate PKC-dependent activation of phagocytic NADPH oxidase. In summary, increased mitochondrial O2·−and impaired buffering of cytosolic Ca2+by dysfunctional mitochondria result in enhanced NADPH oxidase activity, which may contribute to the development of cardiovascular diseases.

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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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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 liver mitochondrial ROS generation to defined steady-state [O2] as low as 0.1 μM. In mitochondria respiring under state 4 (quiescent) or state 3 (ATP turnover) conditions, decreased ROS generation was always observed at low [O2]. It is concluded that the biochemical mechanism to facilitate increased ROS generation in response to hypoxia in cells is not intrinsic to the mitochondrial respiratory chain alone but may involve other factors. The implications for hypoxic cell signaling are discussed.

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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 MitoTEMPO decreased thrombopoiesis, whereas genetically enhancing mtROS by deacetylation-null sirtuin-3 expression increased it. Blocking cytosolic ROS production by NOX inhibitors had no impact. Classification according to the cell roundness index delineated 3 stages of thrombopoiesis in mature MKs. Early-stage round MKs exhibited the highest index, which correlated with low mtROS levels, a mitochondrial tubular network, and the mitochondrial recruitment of the fission activator Drp1. Intermediate MKs at the onset of thrombopoiesis showed high mtROS levels and small, well-delineated mitochondria. Terminal MKs showed the lowest roundness index and long proplatelet extensions. Inhibiting Drp1-dependent mitochondrial fission of mature MKs by Mdivi-1 favored a tubular mitochondrial network and lowered both mtROS levels and intermediate MKs proportion, whereas enhancing Drp1 activity genetically had opposite effects. Reciprocally, quenching mtROS limited mitochondrial fission in round MKs. These data demonstrate a functional coupling between ROS and mitochondrial fission in MKs, which is crucial for the onset of thrombopoiesis. They provide new molecular cues that control initiation of platelet biogenesis and may help elucidate some unexplained thrombocytopenia.

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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 complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

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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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47

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 increasing mitochondrial reactive oxygen species levels. Methods Murine macrophage cells were incubated with iron and then stimulated with lipopolysaccharide. C57BL/6 wild-type mice were intraperitoneally injected with iron and then with lipopolysaccharide. Markers of inflammation and mitochondrial superoxide production were examined. Mitochondrial homeostasis (the balance between mitochondrial biogenesis and destruction) was assessed, as were mitochondrial mass and the proportion of nonfunctional to total mitochondria. Results Iron loading of mice and cells potentiated the inflammatory response to lipopolysaccharide. Iron loading increased mitochondrial superoxide production. Treatment with MitoTEMPO, a mitochondria-specific antioxidant, blunted the proinflammatory effects of iron loading. Iron loading increased mitochondrial mass in cells treated with lipopolysaccharide and increased the proportion of nonfunctional mitochondria. Iron loading also altered mitochondrial homeostasis to favor increased production of mitochondria. Conclusions Acute iron loading potentiates the inflammatory response to lipopolysaccharide, at least in part by disrupting mitochondrial homeostasis and increasing the production of mitochondrial superoxide. Improved understanding of iron homeostasis in the context of acute inflammation may yield innovative therapeutic approaches in perioperative and critically ill patients.

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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 OXPHOS complexes and its functional impact, using the model of isolated brown adipose tissue mitochondria. We demonstrate that biguanides nonspecifically target the activities of all respiratory chain dehydrogenases (mitochondrial NADH, succinate, and glycerophosphate dehydrogenases), but only at very high concentrations (10−2–10−1 M) that highly exceed cellular concentrations observed during the treatment. In addition, these concentrations of biguanides also trigger burst of reactive oxygen species production which, in combination with pleiotropic OXPHOS inhibition, can be toxic for the organism. We conclude that the beneficial effect of biguanides should probably be associated with subtler mechanism, different from the generalized inhibition of the respiratory chain.

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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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