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.
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Authors | P Board, T Nishida, Z Gatmaitan, M Che, I M Arias |
Journal | Hepatology (Baltimore, Md.)
(Hepatology)
Vol. 15
Issue 4
Pg. 722-5
(Apr 1992)
ISSN: 0270-9139 [Print] United States |
PMID | 1551648
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- S-(2,4-dinitrophenyl)glutathione
- Adenosine Triphosphate
- Glutathione
- Glutathione Disulfide
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Topics |
- Adenosine Triphosphate
(pharmacology)
- Animals
- Biological Transport
(drug effects)
- Erythrocyte Membrane
(metabolism)
- Female
- Glutathione
(analogs & derivatives, blood, metabolism)
- Glutathione Disulfide
- Humans
- Hyperbilirubinemia, Hereditary
(blood)
- Jaundice, Chronic Idiopathic
(blood)
- Male
- Rats
- Rats, Inbred Strains
- Substrate Specificity
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