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pubmed-article:1551648pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:1551648pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1551648pubmed:articleTitleErythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the Dubin-Johnson syndrome and in rats with hereditary hyperbilirubinemia.lld:pubmed
pubmed-article:1551648pubmed:affiliationDepartment of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111.lld:pubmed
pubmed-article:1551648pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1551648pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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