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  • 1
    Electronic Resource
    Electronic Resource
    Synthesis of tritiated 4,4′-diisothiocyano-2,2′-stilbene disulfonic acid ([3H]DIDS) and its covalent reaction with sites related to anion transport in human red blood cells (1977)
    Springer
    The journal of membrane biology 33 (1977), S. 311-323 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The potent and specific inhibitor of anion permeability, 4,4′-diisothicyanostilbene-2,2′-disulfonic acid (DIDS) was synthesized in tritiated form ([3H]DIDS) from tritiated 5-nitrotoluene-o-sulfonic acid. Its reactions with and effects on red blood cells were compared with those of a reduced form ([3H]H2DIDS), previously used as a tracer for DIDS. The rate of covalent reaction of [3H]DIDS was substantially faster than that of [3H]H2DIDS at all temperatures tested. With both agents, the rate of reaction was increased in alkaline media, although the response occurred at a lower pH with [3H]DIDS. On the other hand, the relationship of irreversible membrane binding to the degree of inhibition of sulfate fluxes was linear and virtually the same for both agents, with 100% inhibition associated with the binding of approximately 1.2×106 molecules per cell. About 90% of the binding for each probe was to a particular membrane protein, known as band 3, equivalent to about 1 mole of agent per mole of protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869522
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of chloride channels in membrane vesicles from the kidney outer medulla (1989)
    Springer
    The journal of membrane biology 107 (1989), S. 35-42 
    Details
    ISSN: 1432-1424
    Keywords: TALH ; basolateral vesicles ; Cl− transport ; DIDS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The basolateral membrane of the thick ascending loop of Henle (TALH) of the mammalian kidney is highly enriched in Na+/K+ ATPase and has been shown by electrophysiological methods to be highly conductive to Cl−. In order to study the Cl− conductive pathways, membrane vesicles were isolated from the TALH-containing region of the porcine kidney, the red outer medulla, and Cl− channel activity was determined by a36Cl uptake assay where the uptake of the radioactive tracer is driven by the membrane potential (positive inside) generated by an outward Cl− gradient. The accumulation of36Cl− inside the vesicles was found to be dependent on the intravesicular Cl− concentration and was abolished by clamping the membrane potential with valinomycin. The latter finding indicated the involvement of conductive pathways. Cl− channel activity was also observed using a fluorescent potential-sensitive carbocyanine dye, which detected a diffusion potential induced by an imposed inward Cl− gradient. The anion selectivity of the channels was Cl−〉NO 3 − =I−≫ gluconate. Among the Cl− transport inhibitors tested, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPAB), 4,4′-diisothiocyano-stilbene-2,2′-disulfonate (DIDS), and diphenylamine-2-carboxylate (DPC) showed IC50 of 110, 200 and 550 μm, respectively. Inhibition of36Cl uptake by NPPAB and two other structural analogues was fully reversible, whereas that by DIDS was not. The nonreactive analogue of DIDS, 4,4′-dinitrostilbene-2,2′-disulfonate (DNDS), was considerably less inhibitory than DIDS (25% inhibition at 200 μm). The irreversible inhibition by DIDS was prevented by NPPAB, whereas DPC was ineffective, consistent with its low inhibitory potency. It is proposed that NPPAB and DIDS bind to the same or functionally related site on the Cl− channel protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871081
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  • 3
    Electronic Resource
    Electronic Resource
    Vasoconstrictor hormones depolarize renal glomerular mesangial cells by activating chloride channels (1989)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 138 (1989), S. 97-105 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Mesangial cells are smooth muscle-like cells of the renal glomerulus which contract and produce prostaglandins in response to vasopressin and angiotensin. These responses serve to regulate the glomerular capillary filtering surface area. We have used the membrane potential-sensitive fluorescent dye bis-oxonol and the intracellular fluorescent calcium-sensitive probe Indo-1 to study the changes in membrane potential (Em) and intracellular free calcium concentration ([Ca2+ ]i) in cultured rat mesangial cells in response to vasoconstrictor hormones. Basal [Ca2+]i was 227 ± 4 nM, and stimulation by maximal concentrations of either vasopressin or angiotensin resulted in a transient 4-6-fold rise. Resting membrane potential was 45.8 ± 0.9 mV and vasoconstrictor hormones caused a depolarization of 14-18 mV. The following extracellular ion substitutions indicated that chloride efflux was the predominant ion flux responsible for depolarization: (1) depolarization persisted when sodium in the medium was substituted with N-methylglucamine; (2) substitution of medium sodium chloride with sodium gluconate, which enhances the gradient for chloride efflux, augmented vasoconstrictor-stimulated depolarization; (3) suspension of cells in potassium chloride medium resulted in depolarization, following which, stimulation by either vasopressin or angiotensin resulted in hyperpolarization; and (4) this hyperpolarization did not occur when potassium gluconate medium was used to depolarize the cells. The calcium ionophore ionomycin also resulted in membrane depolarization. However, prevention of the rise in [Ca2+]i by prior exposure to ionomycin in calcium-free medium or by loading mesangial cells with the intracellular calcium buffer BAPTA did not abrogate the depolarization response to vasoconstrictor hormones. This indicates that a rise in intracellular calcium is not necessary for depolarization. In contrast, prior depolarization of the cells using varying concentrations of KCl in the external medium, which dissipated the electrochemical gradient for chloride efflux, resulted in a corresponding prolongation of the transient calcium response to vasopressin and angiotensin. These findings indicate that angiotensin and vasopressin depolarize mesangial cells by activating chloride channels and that this activation can occur by both calcium-dependent and -independent mechanisms. In addition, activation of chloride channels with resulting depolarization may serve to modulate the calcium signal.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041380114
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  • 4
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    Transferrin therapy ameliorates disease in β-thalassemic mice (2010)
    Springer Nature
    Details
    Publication Date: 2010-01-24
    Print ISSN: 1078-8956
    Electronic ISSN: 1546-170X
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 5
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    Temporal profiling of redox-dependent heterogeneity in single cells (2018)
    eLife Sciences Publications
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    Publication Date: 2018-06-05
    Description: Cellular redox status affects diverse cellular functions, including proliferation, protein homeostasis, and aging. Thus, individual differences in redox status can give rise to distinct sub-populations even among cells with identical genetic backgrounds. Here, we have created a novel methodology to track redox status at single cell resolution using the redox-sensitive probe Grx1-roGFP2. Our method allows identification and sorting of sub-populations with different oxidation levels in either the cytosol, mitochondria or peroxisomes. Using this approach, we defined a redox-dependent heterogeneity of yeast cells and characterized growth, as well as proteomic and transcriptomic profiles of distinctive redox subpopulations. We report that, starting in late logarithmic growth, cells of the same age have a bi-modal distribution of oxidation status. A comparative proteomic analysis between these populations identified three key proteins, Hsp30, Dhh1, and Pnc1, which affect basal oxidation levels and may serve as first line of defense proteins in redox homeostasis.
    Electronic ISSN: 2050-084X
    Topics: Biology , Medicine , Natural Sciences in General
    Published by eLife Sciences Publications
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  • 6
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    Cell functions impaired by frataxin deficiency are restored by drug-mediated iron relocation (2008)
    American Society of Hematology
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    Publication Date: 2008-12-15
    Description: Various human disorders are associated with misdistribution of iron within or across cells. Friedreich ataxia (FRDA), a deficiency in the mitochondrial iron-chaperone frataxin, results in defective use of iron and its misdistribution between mitochondria and cytosol. We assessed the possibility of functionally correcting the cellular properties affected by frataxin deficiency with a siderophore capable of relocating iron and facilitating its metabolic use. Adding the chelator deferiprone at clinical concentrations to inducibly frataxin-deficient HEK-293 cells resulted in chelation of mitochondrial labile iron involved in oxidative stress and in reactivation of iron-depleted aconitase. These led to (1) restoration of impaired mitochondrial membrane and redox potentials, (2) increased adenosine triphosphate production and oxygen consumption, and (3) attenuation of mitochondrial DNA damage and reversal of hypersensitivity to staurosporine-induced apoptosis. Permeant chelators of higher affinity than deferiprone were not as efficient in restoring affected functions. Thus, although iron chelation might protect cells from iron toxicity, rendering the chelated iron bioavailable might underlie the capacity of deferiprone to restore cell functions affected by frataxin deficiency, as also observed in FRDA patients. The siderophore-like properties of deferiprone provide a rational basis for treating diseases of iron misdistribution, such as FRDA, anemia of chronic disease, and X-linked sideroblastic anemia with ataxia.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 7
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    Redistribution of accumulated cell iron: a modality of chelation with therapeutic implications (2008)
    American Society of Hematology
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    Publication Date: 2008-02-01
    Description: Various pathologies are characterized by the accumulation of toxic iron in cell compartments. In anemia of chronic disease, iron is withheld by macrophages, leaving extracellular fluids iron-depleted. In Friedreich ataxia, iron levels rise in the mitochondria of excitable cells but decrease in the cytosol. We explored the possibility of using deferiprone, a membrane-permeant iron chelator in clinical use, to capture labile iron accumulated in specific organelles of cardiomyocytes and macrophages and convey it to other locations for physiologic reuse. Deferiprone's capacity for shuttling iron between cellular organelles was assessed with organelle-targeted fluorescent iron sensors in conjunction with time-lapse fluorescence microscopy imaging. Deferiprone facilitated transfer of iron from extracellular media into nuclei and mitochondria, from nuclei to mitochondria, from endosomes to nuclei, and from intracellular compartments to extracellular apotransferrin. Furthermore, it mobilized iron from iron-loaded cells and donated it to preerythroid cells for hemoglobin synthesis, both in the presence and in the absence of transferrin. These unique properties of deferiprone underlie mechanistically its capacity to alleviate iron accumulation in dentate nuclei of Friedreich ataxia patients and to donate tissue-chelated iron to plasma transferrin in thalassemia intermedia patients. Deferiprone's shuttling properties could be exploited clinically for treating diseases involving regional iron accumulation.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 8
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    Comparison of Overt and Cryptic Labile Plasma Iron In Thalassemia Patients In Israel and Gaza-Palestine (2010)
    American Society of Hematology
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    Publication Date: 2010-11-19
    Description: Abstract 5166 Background. Systemic iron overload (SIO) is characterized by persistently high levels of plasma iron that often surpass transferrin's (Tf) binding capacity and generate chemical forms identified as non-Tf bound iron (NTBI). These forms have been perceived as: a. clinically important indicators of SIO per se and of impending organ damage, because cells chronically exposed to iron overloaded plasma attain iron levels and ensuing ROS formation that override their antioxidant capacities and b. as pharmacological targets for chelation and thereby of prevention of tissue iron overload. However, NTBI determination in the clinical setting has been confounded by the chemical heterogeneity of iron forms found in fluids like plasma/sera of SIO patients, the presence of residual amounts of undefined chelates or chelators and the need to dislodge NTBI from native ligands with agents that facilitate its detection. We have assayed the overt forms of NTBI that represent the native pool of labile (= redox-active, chelatable and membrane permeant) iron in plasma/serum. We defined it as ‘labile plasma iron' or LPI and analyzed it by the Aferrix FeROS™ test (1) and used it to asses chelation regimens in their ability to maintain patients' plasma at relatively low (basal) LPI levels (10 hrs drug washout, as described for LPI (1,2) and DCI (4); for LPIplus, the LPI test was conducted in the presence of 0.5 mM NTA. Results. As shown previously (2,4), LPI was detected only in patients with 〉70% Tf-saturation. In HMC, the mean LPI of n=18 patients rose from 0.51±0.41 μ M to 1.00 ±0.46 μ M in the presence of NTA, matching the DCI level of 0.91±0.7 μ M. The LPI rise was detected in 12/15 (= 80%) of samples with LPI〉0.4 μ M (≂p 66% of the entire cohort). Thus, despite chelation, a substantial number of patients had relatively low but significant levels of both overt and cryptic NTBI. Among the 3 patients with no significant LPI or DCI (0.2-0.4 μ M), 2/3 became LPI positive (0.6-0.8 μ M) when tested with NTA. Unexpectedly, in EMC-Gaza, among 20 transfused unchelated patients with serum ferritins 〉 5000 ng/ml and Tf saturation 〉100%, 8/20 of them (≂p 40%) had undetectable levels of overt LPI but substantial cryptic NTBI. In the remaining 12/20, the mean overt LPI of 0.69±0.65 μ M rose significantly (p
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 9
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    Down Regulation of Hepcidin and Haemojuvelin Expression in the Hepatocyte Cell-Line HepG2 Induced by Thalassaemic Sera. (2006)
    American Society of Hematology
    Details
    Publication Date: 2006-11-16
    Description: β-thalassaemia represents a group of diseases, in which ineffective erythropoiesis is accompanied by iron overload. In a mouse model of β-thalassaemia we observed that the liver expresses relatively low levels of hepcidin, which is a key factor in the regulation of iron absorption by the gut and of iron recycling by the reticuloendothelial system. We hypothesized that despite the overt iron overload, a putative plasma factor found in β-thalassaemia might suppress liver hepcidin expression. We therefore compared sera from β-thalassaemia and haemochromatosis (C282Y mutation) patients with those of healthy individuals in terms of their capacity to evoke changes in expression of key genes of iron metabolism in human HepG2 hepatoma cells. Sera from β-thalassaemia major patients evoked a major decrease in hepcidin (HAMP) and lipocalin2 (oncogene 24p3) (LCN2) expression, as well as a moderate decrease in haemojuvelin (HFE2) expression, compared to sera from healthy individuals. Significant correlation was found between the degree of downregulation of HAMP and HFE2 evoked by b-thalassaemia major sera (r=0.852, p
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 10
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    Action of chelators in iron-loaded cardiac cells: accessibility to intracellular labile iron and functional consequences (2006)
    American Society of Hematology
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    Publication Date: 2006-11-01
    Description: Labile iron in hemosiderotic plasma and tissue are sources of iron toxicity. We compared the iron chelators deferoxamine, deferiprone, and deferasirox as scavengers of labile iron in plasma and cardiomyocytes at therapeutic concentrations. This comprised chelation of labile plasma iron (LPI) in samples from thalassemia patients; extraction of total cellular iron; accessing labile iron accumulated in organelles and preventing formation of reactive-oxidant species; and restoring impaired cardiac contractility. Neonatal rat cardiomyocytes were used for monitoring chelator extraction of LCI (labile cell iron) as 59Fe; assessing in situ cell iron chelation by epifluorescence microscope imaging using novel fluorescent sensors for iron and reactive oxygen species (ROS) selectively targeted to organelles, and monitoring contractility by time-lapse microscopy. At plasma concentrations attained therapeutically, all 3 chelators eliminated LPI but the orally active chelators rapidly gained access to the LCI pools of cardiomyocytes, bound labile iron, attenuated ROS formation, extracted accumulated iron, and restored contractility impaired by iron overload. The effect of deferoxamine at therapeutically relevant concentrations was primarily by elimination of LPI. The rapid accessibility of the oral chelators deferasirox and deferiprone to intracellular labile iron compartments renders them potentially efficacious for protection from and possibly reversal of cardiac damage induced by iron overload.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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