Relevant bibliographies by topics / Mitochondrial reactive oxygen species

Academic literature on the topic 'Mitochondrial reactive oxygen species'

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Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "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 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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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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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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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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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 involvement of the oxidative stress in the regulation of some actors of mitochondrial biogenesis.
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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 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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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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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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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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Dissertations / Theses on the topic "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 H2O2 or when they generate ROS endogenously. Using isolated mitochondria, those proteins that are particularly sensitive to low concentrations of H2O2 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 dehydrogenase complex. Next the mechanisms by which ROS selectively oxidise mitochondrial thiol proteins were investigated; it was determined that H2O2 generated by the electron transport chain may either oxidise mitochondrial thiol proteins directly or indirectly, through oxidation of the peroxiredoxin and thioredoxin redox couples. To determine if ROS generated by mitochondria might act as a redox signal by altering the functions of mitochondrial proteins, the effect of protein thiol oxidation was tested on the activity of two proteins: pyruvate dehydrogenase kinase and propionyl-CoA carboxylase. Loss of pyruvate dehydrogenase kinase and propionyl-CoA carboxylase activity correlated with protein thiol oxidation and was very sensitive to ROS, suggesting a plausible mechanism of redox regulation of these proteins in vivo. Lastly, glutathionylation of complex I was investigated in intact mitochondria exposed to a glutathione oxidant; two cysteine residues on the 75 kDa subunit of complex I were shown to become glutathionylated. The functional effect of glutathionylation of these two cysteine residues on complex I activity is currently under investigation.
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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
Ph.D.
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 novel hypothesis that mtROS serve as signaling mediators for LPC-induced EC activation. Using electron spin resonance and flow cytometry with mtROS-specific fluorescence probe MitoSOX, we found that several LPC species including LPC 16:0, 18:0, and 18:1 induced mtROS in human primary aortic ECs (HAECs). Mechanistically, our analysis using confocal microscopy and Seahorse XF96 mitochondrial function analyzer showed that LPC induced mtROS via increasing mitochondrial calcium-mediated increase of mitochondrial respiration. In addition, we found that mtROS scavenger MitoTEMPO abolished LPC-induced EC activation by downregulating Intercellular adhesion molecule 1 (ICAM-1) in HAECs. Moreover, our analysis with mass spectrometer analysis of histone H3 lysine acetylation and electrophoretic mobility shift assay (EMSA) showed that MitoTEMPO acts by blocking LPC-induced histone H3 lysine 14 acetylation (H3K14ac) and nuclear translocation of pro-inflammatory transcription factor activator protein-1 (AP-1). Remarkably, all the above effects can be inhibited by anti-inflammatory cytokines interleukin (IL-35) and IL-10. Our results indicate that mtROS are responsible for LPC-induced EC activation, which can be inhibited by anti-inflammatory cytokines. MtROS targeting therapies and anti-inflammatory cytokines such as IL-35 may serve as novel therapeutic targets for vascular inflammation and cardiovascular diseases. The studies in this dissertation were supported by grants from the National Institutes of Health (NIH) funded to Dr. Xiao-Feng Yang.
Temple University--Theses
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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 in which mitochondrial ROS may behave as a signal is by altering the activity of AMP-activated protein kinase (AMPK), a key metabolic sensor and regulator of cell metabolism, which is activated when cellular ATP levels decrease during energy demand. Mitochondria can signal to AMPK via the magnitude of the cellular ATP/AMP and ATP/ADP ratios, which alter in response to mitochondrial function. Our view is mitochondria may also signal to AMPK via ROS. Important studies have helped to clarify the role of exogenous or cytosolic ROS in AMPK regulation. However, the effects of mitochondrial ROS on AMPK activity, specifically that generated by complex I, remain unclear and is the main focus of this thesis. I characterized the effects of exogenous H2O2 on cellular AMPK activity, ATP/ADP ratios and cellular redox state in a cell model. I then compounded this with selective mitochondria generated ROS by the mitochondria-targeted redox-cycler, MitoParaquat (MPQ). AMPK activity appeared to correlate with decreasing cell ATP/ADP ratios, indicating that both sources of ROS primarily activate AMPK in an AMP/ADP-dependent mechanism. In parallel, I developed an approach for analyzing the redox state of candidate proteins, an important step in determining if a protein is directly regulated by ROS. I also initiated development of a cell model for studying the downstream effects of mitochondrial ROS production by RET, by expressing alternative respiratory enzymes in a mammalian cell line.
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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 mitochondrial superoxide. The current study aimed to investigate if modulation of mitochondrial reactive oxygen species signalling is a general mechanism for senescence induction in human VSMC. The electron transport chain inhibitors Antimycin A and rotenone and the mitochondrial redox cycler, MitoParaquat all stimulated SIPS in VSMC. Interestingly, Antimycin A and rotenone also lead to a reduction in overall H₂O₂ levels suggesting a possible protective mechanism and highlighting the complexity of the signalling mechanism involving mitochondrial oxidants. qPCR Analysis suggested that changes in antioxidant gene expression do not account for the reduction in peroxide levels. Although there was no evidence that Angiotensin II induced senescence in human coronary artery SMC, there was evidence for enhanced mitochondrial hydrogen peroxide production. Senescent cells acquire a senescence associated secretory phenotype (SASP). To determine the composition of VSMC SASP, the tryptically digested secretome of conditioned media was analysed by LC-MS/MS. Bioinformatic analysis identified the NRF2-mediated oxidative stress response pathway and several endogenous antioxidants as amongst the affected responses in the aged VSMC secretome. These new data suggest that senescent VSMC produce a SASP that has multiple effects on neighbouring cell types including the induction of cell senescence and death; but also elements that might serve to preserve cell integrity and function and may limit the expression of a pro-inflammatory phenotype.
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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 mitochondrial function and oxidative stress. Results of experiments investigating mitochondrial integrity, cell viability, and ROS levels in Trx-2(-/-) mouse embryonic fibroblasts (MEFs), and results from Trx-2 siRNA MEFs, are similar to findings of knockouts in previously reported proteins that function in mitochondrial respiration and support the involvement of Trx-2 in this process. Mitochondrial ROS have also been implicated as major secondary messengers in cell signaling. Results reported here using cancer cells and cancer cells depleted of mitochondrial DNA, which consequently produce few ROS, have indicated that mitochondrial ROS produced in hypoxia are necessary for HRE and ARE activation, and are fundamental in the activation of SP-1 during reoxygenation. However, mitochondrial ROS are not required for HIF-1α protein expression in hypoxia, indicating a unique relationship between HIF-1α, hypoxia, and mitochondrial ROS.
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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 responsible for this feedback effect is not known. Superoxide was excluded in earlier work on the basis that it does not activate PKCε and does not induce mitoKATP opening.To further examine the identity of the signaling ROS, respiring rat heart mitochondria were preincubated with ATP and diazoxide to induce the phosphorylation-dependent open state, together with agents that may interrupt feedback activation of mitoKATP by ROS scavenging or by blocking ROS transformations. Swelling assays of the preincubated mitochondria revealed that dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, trolox, and bromoenol lactone (BEL) each blocked the ROS-dependent open state but catalase did not interfere with this step. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO• excludes H2O2 as the endogenous signaling ROS and focuses attention on HO•. In support of the hypothesis that HO• is required, we also found that HO•-scavenging by DMF blocked cardioprotection by both ischemic preconditioning and diazoxide in the Langendorff perfused rat heart. HO• itself cannot act as a signaling molecule, because its lifetime is too short and it reacts immediately with nearest neighbor phospholipids and proteins. Therefore, these findings point to a product of phospholipid peroxidation, such as hydroperoxy-fatty acids. Indeed, this hypothesis was supported by the finding that hydroperoxylinoleic acid (LAOOH) opens the ATP-inhibited mitoKATP in isolated mitochondria. This effect was blocked by the specific PKCε inhibitor peptide εV1-2, showing that LAOOH activates the mitoKATP-associated PKCε. During ischemia, catabolism of mitochondrial phospholipids is accelerated, causing accumulation of plasmalogens and free fatty acids (FA) in the heart by the action of calcium independent phospholipases A2 (iPLA2). We first assessed the role of FAs and hydroxy FAs on mitoKATP opening and cardioprotection. Swelling assays of isolated rat heart mitochondria showed that naturally formed free FAs inhibit mitoKATP opening and that they are more potent inhibitors of the pharmacological open state of mitoKATP than the phosphorylation-dependent open state. That is, sustained mitoKATP opening induced by the phosphorylation-dependent feedback loop is more resistant to FA inhibition than direct mitoKATP opening by a potassium channel opener. Moreover, rat hearts perfused with micromolar concentrations of FA were resistant to cardioprotection by diazoxide or ischemic preconditioning. Racemic bromoenol lactone (BEL), a selective inhibitor of iPLA2, confers protection to otherwise untreated Langendorff perfused hearts by preventing ischemic FA release. To bring this story full circle, BEL blocks protection afforded by preconditioning and postconditioning by preventing the iPLA2-mediated release of FAOOH generated in the conditioned heart. HO• resulting from mitoKATP opening oxidizes polyunsaturated fatty acid components of the membrane phospholipids, resulting in a peroxidized side chain. FAOOH must be released in order to act on the mitochondrial PKCε, and this is achieved by the action of iPLA2. iPLA2 is essential for most modes of cardioprotection because it catalyzes the release of FAOOH. This fully supports the hypothesis that the second messenger of cardioprotective ROS-mediated signaling is hydroperoxy fatty acid (FAOOH), a downstream oxidation product of HO•.
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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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Books on the topic "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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Book chapters on the topic "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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Conference papers on the topic "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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Reports on the topic "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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