Erythrocyte membrane transport of glutathione conjugates and oxidized glutathione in the dubin‐johnson syndrome and in rats with hereditary hyperbilirubinemia
Philip Board, Toshirou Nishida, Zenaida Gatmaitan, Mingxin Che, Irwin M. Arias – 1 April 1992 – 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.