Efflux of glutathione and glutathione complexes from human erythrocytes in response to vanadate
Yükleniyor...
Dosyalar
Tarih
2013
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Academic Press Inc Elsevier Science
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
The 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.
Açıklama
Anahtar Kelimeler
Vanadate, Glutathione efflux, Human erythrocytes, Membrane transport
Kaynak
Blood Cells Molecules and Diseases
WoS Q Değeri
Q3
Scopus Q Değeri
Q2
Cilt
50
Sayı
1
