Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the Dubin-Johnson syndrome and in rats with hereditary hyperbilirubinemia.

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.

• 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.)

Chemical References

• S-(2,4-dinitrophenyl)glutathione
• Adenosine Triphosphate
• Glutathione
• Glutathione Disulfide

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