Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate

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dc.contributor.authorCakir, Yeliz
dc.contributor.authorYildiz, Deniz
dc.date.accessioned2024-09-18T21:00:32Z
dc.date.available2024-09-18T21:00:32Z
dc.date.issued2013
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractThe main objective of the present study was to investigate if vanadate is extruded from the cells in a glutathione dependent manner resulting in the appearance of extracellular glutathione and complexes of glutathione with vanadium. Vanadate significantly depleted intracellular non-protein sulfhydryl (NPSH) levels in a time- and concentration-dependent manner. The intracellular NPSH level was decreased to 0.0 +/- 0.0 mu mol/ml erythrocyte when exposed to 10 mM of vanadate for 4 h. Extracellular NPSH level was increased concomitantly with the intracellular decrease and reached to 0.1410 +/- 0.005 mu mol/ml erythrocyte in 4 h. Intracellular decrease and extracellular increase in NPSH levels were significantly inhibited in the presence of DIDS, a chloride-bicarbonate exchanger which also mediates phosphate and arsenate transport in erythrocytes. In parallel with the increase in extracellular NPSH levels, significant increases in extracellular glutathione levels were detected following exposure to vanadate. Extracellular glutathione levels reached to 0.0150 +/- 0.0.001, 0.0330 +/- 0.001, and 0.0576 +/- 0.002 mu mol/ml erythrocyte with 1, 5, and 10 mM of vanadate respectively. Dimercaptosuccinic acid treatment of supematants significantly increased the glutathione levels measured in the extracellular media. Utilization of MK571 an MRP inhibitor decreased the rate of glutathione efflux from erythrocytes suggesting a role for this membrane transporter in the process. A known methylation inhibitor periodate oxidized adenosine decreased the rate of glutathione efflux from erythrocytes. This observed decrease in extracellular GSH levels suggests that GSH release partly requires a proper cellular methylation process and that part of GSH detected in the extracellular media may arise from GSH-vandium complexes. The results of the present study indicate that human erythrocyte efflux glutathione in reduced free form and in conjugated form/s that can be recovered with dimercaptosuccinic acid when exposed to vanadate. (C) 2012 Elsevier Inc. All rights reserved.en_US
dc.identifier.doi10.1016/j.bcmd.2012.07.001
dc.identifier.endpage7en_US
dc.identifier.issn1079-9796
dc.identifier.issn1096-0961
dc.identifier.issue1en_US
dc.identifier.pmid22824382en_US
dc.identifier.scopus2-s2.0-84869878959en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1en_US
dc.identifier.urihttps://doi.org/10.1016/j.bcmd.2012.07.001
dc.identifier.urihttps://hdl.handle.net/20.500.12483/12745
dc.identifier.volume50en_US
dc.identifier.wosWOS:000312237400001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.relation.ispartofBlood Cells Molecules and Diseasesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectVanadateen_US
dc.subjectGlutathione effluxen_US
dc.subjectHuman erythrocytesen_US
dc.subjectMembrane transporten_US
dc.titleEfflux of glutathione and glutathione complexes from human erythrocytes in response to vanadateen_US
dc.typeArticleen_US

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