Redox modulation of intracellular free calcium concentration in thyroid FRTL-5 cells: evidence for an enhanced extrusion of calcium

Törnquist, Kid; VAINIO, Petri; Titievsky, Alexey; Dugué, Benoît; TUOMINEN, Raimo

doi:10.1042/0264-6021:3390621

Cited by 9 publications

(12 citation statements)

References 29 publications

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“…Indeed, a recent report has shown an oxidant-dependent activation of plasmamembrane Ca-ATPases through phosphorylation. The activated enzyme caused an increased efflux of Ca 2+ thereby decreasing agonist-induced intracellular Ca 2+ levels [47].…”

Section: Discussionmentioning

confidence: 99%

H2O2 impairs inflammatory mediator release from immunologically stimulated RBL-2H3 cells through a redox-sensitive, calcium-dependent mechanism

Guérin-Marchand¹,

Sénéchal²,

Pelletier³

et al. 2001

Inflamm. res.

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While in many cells H2O2 induces potent inflammatory responses we show that it can be an anti-inflammatory agent by not only inhibiting the release of preformed mediators but also by affecting the secretion of newly synthesized TNF-alpha. Inhibition is a consequence of the profound effect on intracellular calcium levels. The activation of an intracellular oxidative burst by FcepsilonRI aggregation and the sensitivity of intracellular responses to redox-altering agents point to an important regulatory mechanism of mast cell responses in inflammatory tissues.

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Section: Discussionmentioning

confidence: 99%

H2O2 impairs inflammatory mediator release from immunologically stimulated RBL-2H3 cells through a redox-sensitive, calcium-dependent mechanism

Guérin-Marchand¹,

Sénéchal²,

Pelletier³

et al. 2001

Inflamm. res.

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“…Several years later Törnquist et al confirmed the finding that SOCE is inhibited by thiol-modifying oxidizing agents such as thimerosal, tBHP and H 2 O 2 (300 M). However, their results suggest that these effects are mediated through activation of protein kinase C (PKC) [176,177]. Vanadate and its derivative pervanadate obtained from a chemical reaction with H 2 O 2 are well established as thiol modifying agents and also implicated in modulating SOCE.…”

Section: Reactive Oxygen Species Effects On Soce and Crac/orai Channelsmentioning

confidence: 99%

“…Hawkins et al [188] studied redox mediated activation of STIM1 and found that oxidative stress leads to gluthationylation of STIM1's cysteine 56, triggering STIM1 oligomerization and punctae [171][172][173][174][175][176][177][180][181][182][183][184][185][186]189,[192][193][194][195][203][204][205][206][207][208][209][210][211][212][213][214][215][216][217][218] BSO, buthionine sulfoximine; DEANO, 2-(N,N-diethylamino)diazenolate-2-oxide; FRTL-5, fischer rat thyroid low serum 5%; GEA3162, 1,2,3,4,-oxatriazolium, 5-amino-3-(3,4-dichlorophenyl)-chloride; HEK, human embryonic kidney; IP3R, IP3 receptor; Jurkat, human leukemic T cell line; MEF, mouse embryonic fibroblasts; RBL, rat basophilic leukemia; RyR, ryanodine receptor; SH-SY5Y, human neuroblastoma cell line; SNP, sodium nitroprusside; tBHP, tert-butylhydroperoxide.…”

Section: Reactive Oxygen Species Effects On Soce and Crac/orai Channelsmentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

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a b s t r a c tReactive oxygen species (ROS) are increasingly recognized as second messengers in many cellular processes. While high concentrations of oxidants damage proteins, lipids and DNA, ultimately resulting in cell death, selective and reversible oxidation of key residues in proteins is a physiological mechanism that can transiently alter their activity and function. Defects in ROS producing enzymes cause disturbed immune response and disease.Changes in the intracellular free Ca 2+ concentration are key triggers for diverse cellular functions. Ca 2+ homeostasis thus needs to be precisely tuned by channels, pumps, transporters and cellular buffering systems. Alterations of these key regulatory proteins by reversible or irreversible oxidation alter the physiological outcome following cell stimulation. It is therefore necessary to understand which proteins are regulated and if this regulation is relevant in a physiological-and/or pathophysiological context. Because ROS are inherently difficult to identify and to measure, we first review basic oxygen redox chemistry and methods of ROS detection with special emphasis on electron paramagnetic resonance (EPR) spectroscopy. We then focus on the present knowledge of redox regulation of Ca 2+ permeable ion channels such as voltage-gated (CaV) Ca 2+ channels, transient receptor potential (TRP) channels and Orai channels.© 2011 Elsevier Ltd. All rights reserved. Basic redox chemistry of oxygenMany chemical processes are linked to the exchange of electrons between two or more molecular entities. The transfer of one (or more) electron(s) is associated with oxidation (loss of electron) and reduction (gain of electron) of the components. Such reactions are also known as redox reactions. The processes of reactive oxygen species (ROS) formation and elimination are exclusively of redox nature.Molecular oxygen is the precursor of all ROS. It contains two unpaired electrons in separate (antibonding) orbitals in its outer electron sphere and is thus, by definition, a radical. Radicals have at least one unpaired electron in their orbital system and usually show high reactivity; transition metal ions also may have unpaired electrons, but are not called radicals. Although having radical character, molecular oxygen is chemically rather inert (luckily!), because high * Corresponding authors at: Institut für Biophysik, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: +49 6841 1626453; fax: +49 6841 1626060.E-mail addresses: ivan.bogeski@uks.eu (I. Bogeski), barbara.niemeyer@uks.eu (B.A. Niemeyer).

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“…This mobilizatio n of calcium can in turn modulate a number of cell functions. Tornquist et al (1999) found that thimerosal mobilized sequestered calcium and evoked modest store-dependent calcium entry in thyroid F RTL-5 cells. The mechanism of action was suggested to be mediated via activation of protein kinase C, as thimerosal potently stimulated the bonding of [3H ]phorbol-12,13-dibutyrate and was without effect on store-operated calcium entry in cells treated with staurosporine or in cells with downregulated protein kinase C. Whole cell patch clamping experiments revealed that thimerosal did not depolarize the membrane potential.…”

Section: Mechanisms Of Toxicitymentioning

confidence: 98%

Organic mercury compounds: human exposure and its relevance to public health

2002

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Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes, and the effects of such exposure depend upon both the type of mercury to which exposed and the magnitude of the exposure. In general, the effects of exposure to organic mercury are primarily neurologic, while a host of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal. While the primary source of exposure to organic mercury for most populations is the consumption of methylmercury-contaminated fish and shellfish, there are a number of other organomercurials to which humans might be exposed. The antibacterial and antifungal properties of organomercurials have resulted in their long use as topical disinfectants (thimerosal and merbromin) and preservatives in medical preparations (thimerosal) and grain products (both methyl and ethyl mercurials). Phenylmercury has been used in the past in paints, and dialkyl mercurials are still used in some industrial processes and in the calibration of certain analytical laboratory equipment. The effects of exposure to different organic mercurials by different routes of exposure are summarized in this article.

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Redox modulation of intracellular free calcium concentration in thyroid FRTL-5 cells: evidence for an enhanced extrusion of calcium

Cited by 9 publications

References 29 publications

H2O2 impairs inflammatory mediator release from immunologically stimulated RBL-2H3 cells through a redox-sensitive, calcium-dependent mechanism

H2O2 impairs inflammatory mediator release from immunologically stimulated RBL-2H3 cells through a redox-sensitive, calcium-dependent mechanism

Redox regulation of calcium ion channels: Chemical and physiological aspects

Organic mercury compounds: human exposure and its relevance to public health

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