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Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the dubin‐johnson syndrome and in rats with hereditary hyperbilirubinemia

Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the... The Dubin‐Johnson syndrome is manifested by conjugated hyperbilirubinemia and pigment accumulation in hepatocellular lysosomes. The TR‐ rat model is a phenotypic model of the Dubin‐Johnson syndrome and is characterized by defective ATP‐dependent transport of a group of nonbile acid organic anions, including glutathione‐S‐conjugates and oxidized glutathione, across the bile canaliculus. Similar ATP‐dependent transport mechanisms have been described in erythrocytes. Intact erythrocytes and inverted erythrocyte membrane vesicles from Dubin‐Johnson patients, TR‐rats and appropriate controls were studied with regard to ATP‐dependent transport of dinitrophenyl glutathione and oxidized glutathione. No significant differences were observed, indicating that the erythrocyte and canalicular ATP‐dependent transporters for these substrates are functionally and potentially genetically distinct. (Hepatology 1992;15:722–725). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hepatology Wolters Kluwer Health

Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the dubin‐johnson syndrome and in rats with hereditary hyperbilirubinemia

Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the dubin‐johnson syndrome and in rats with hereditary hyperbilirubinemia

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References (30)

Publisher
Wolters Kluwer Health
Copyright
Copyright © 1992 Wiley Subscription Services, Inc.
ISSN
0270-9139
eISSN
1527-3350
DOI
10.1002/hep.1840150428
Publisher site
See Article on Publisher Site

Abstract

The Dubin‐Johnson syndrome is manifested by conjugated hyperbilirubinemia and pigment accumulation in hepatocellular lysosomes. The TR‐ rat model is a phenotypic model of the Dubin‐Johnson syndrome and is characterized by defective ATP‐dependent transport of a group of nonbile acid organic anions, including glutathione‐S‐conjugates and oxidized glutathione, across the bile canaliculus. Similar ATP‐dependent transport mechanisms have been described in erythrocytes. Intact erythrocytes and inverted erythrocyte membrane vesicles from Dubin‐Johnson patients, TR‐rats and appropriate controls were studied with regard to ATP‐dependent transport of dinitrophenyl glutathione and oxidized glutathione. No significant differences were observed, indicating that the erythrocyte and canalicular ATP‐dependent transporters for these substrates are functionally and potentially genetically distinct. (Hepatology 1992;15:722–725).

Journal

HepatologyWolters Kluwer Health

Published: Apr 1, 1992

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