MRP2-Mediated Reduced Glutathione Transport in Protection Against Oxidant Stress

2003 ◽  
Vol 9 (3-4) ◽  
pp. 215-228 ◽  
Author(s):  
Nazzareno Ballatori ◽  
Christine L. Hammond ◽  
Jennifer B. Cunningham
2000 ◽  
Vol 1464 (2) ◽  
pp. 207-218 ◽  
Author(s):  
Aravind V. Mittur ◽  
Neil Kaplowitz ◽  
Ellis S. Kempner ◽  
Murad Ookhtens

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 507-515 ◽  
Author(s):  
JA Warth ◽  
DL Rucknagel

Abstract An increase in the number of irreversibly sickled cells (ISCs) in pain crisis has been found by some investigators but not others. We have used the technique of discontinuous arabinogalactan density-gradient ultracentrifugation of whole blood to study ISCs from patients with sickle cell anemia (SCA) during pain crisis and again when pain free (5- 331 days after crisis). Nine patients have been studied through ten episodes of pain crisis. Five layers with densities from 1.128 g/mL to 1.158 g/mL have been used. Careful classification of the cells using Nomarsky optics demonstrated highly significant changes occurring in the layers of the gradient. The changes involve the appearance of an increased percentage of echinocytic ISCs and echinocytic cells that were not ISCs, especially in the denser gradient layers, during crisis, and their replacement by normal-appearing discocytes in the pain-free state. There was no change in ISCs that were not echinocytic. Data collected previously demonstrated that reduced glutathione activity correlated with increased echinocytosis in our gradient layers. This indicates that the echinocytic change may occur as a result of oxidant stress. Hemoglobin F levels and the percentage of hemoglobin F from reticulocytes showed no consistent change to coincide with the rise in normal-appearing discocytes in the lightest layers after crisis. Our data indicate that pain crisis occurs in association with an echinocytic change, which may be induced by oxidant injury. The rise in normal-appearing cells after crisis may reflect increased hemoglobin F production in some patients but mainly relates to the disappearance of these echinocytic erythrocytes.


2005 ◽  
Vol 204 (3) ◽  
pp. 238-255 ◽  
Author(s):  
Nazzareno Ballatori ◽  
Christine L. Hammond ◽  
Jennifer B. Cunningham ◽  
Suzanne M. Krance ◽  
Rosemarie Marchan

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 507-515 ◽  
Author(s):  
JA Warth ◽  
DL Rucknagel

An increase in the number of irreversibly sickled cells (ISCs) in pain crisis has been found by some investigators but not others. We have used the technique of discontinuous arabinogalactan density-gradient ultracentrifugation of whole blood to study ISCs from patients with sickle cell anemia (SCA) during pain crisis and again when pain free (5- 331 days after crisis). Nine patients have been studied through ten episodes of pain crisis. Five layers with densities from 1.128 g/mL to 1.158 g/mL have been used. Careful classification of the cells using Nomarsky optics demonstrated highly significant changes occurring in the layers of the gradient. The changes involve the appearance of an increased percentage of echinocytic ISCs and echinocytic cells that were not ISCs, especially in the denser gradient layers, during crisis, and their replacement by normal-appearing discocytes in the pain-free state. There was no change in ISCs that were not echinocytic. Data collected previously demonstrated that reduced glutathione activity correlated with increased echinocytosis in our gradient layers. This indicates that the echinocytic change may occur as a result of oxidant stress. Hemoglobin F levels and the percentage of hemoglobin F from reticulocytes showed no consistent change to coincide with the rise in normal-appearing discocytes in the lightest layers after crisis. Our data indicate that pain crisis occurs in association with an echinocytic change, which may be induced by oxidant injury. The rise in normal-appearing cells after crisis may reflect increased hemoglobin F production in some patients but mainly relates to the disappearance of these echinocytic erythrocytes.


1993 ◽  
Vol 268 (4) ◽  
pp. 2324-2328
Author(s):  
J.C. Fernández-Checa ◽  
J.R. Yi ◽  
C. Garcia-Ruiz ◽  
Z. Knezic ◽  
S.M. Tahara ◽  
...  

1993 ◽  
Vol 75 (2) ◽  
pp. 566-572 ◽  
Author(s):  
C. A. Viguie ◽  
B. Frei ◽  
M. K. Shigenaga ◽  
B. N. Ames ◽  
L. Packer ◽  
...  

We tested whether consecutive days of prolonged submaximal exercise would result in oxidant stress sufficient to alter blood antioxidant profiles, progressively change and exhaust blood and plasma antioxidants, and damage RNA. Eleven moderately trained males (24.3 +/- 1.1 yr) exercised 90 min at 65% peak O2 uptake on a cycle ergometer for 3 consecutive days. During day 1 exercise, blood reduced glutathione (GSH) declined 55 +/- 10% and oxidized glutathione (GSSG) increased 28 +/- 7% within 15 min. Total blood glutathione did not significantly change during exercise. GSH levels returned to baseline after 15 min of recovery. On day 3, preexercise GSH and GSSG levels were not significantly different from day 1 preexercise values; essentially similar results were obtained during exercise and recovery. During day 1 exercise, plasma total ascorbate (ascorbate + dehydroascorbate) increased from 53.8 +/- 9.3 to 59.0 +/- 11.3 microM, and percent reduced ascorbate increased from 77.6 +/- 9.3 to 87.3 +/- 9.7%. During day 3 exercise, plasma ascorbate changes were similar to those on day 1. Plasma vitamin E did not change due to exercise on either day 1 or 3. RNA adducts, urinary 8-hydroxyguanosine, did not change significantly due to exercise. Observed increases in GSH oxidation indicate the presence of oxidant stress during prolonged submaximal exercise. Similar redox changes on consecutive days of exercise, with recovery to preexercise values within 15 min, indicate no evidence of persistent or cumulative exercise effects on blood glutathione redox status.(ABSTRACT TRUNCATED AT 250 WORDS)


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