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Research Article Free access | 10.1172/JCI114189

Hepatobiliary transport of glutathione and glutathione conjugate in rats with hereditary hyperbilirubinemia.

R P Elferink, R Ottenhoff, W Liefting, J de Haan, and P L Jansen

Division of Gastrointestinal and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands.

Find articles by Elferink, R. in: PubMed | Google Scholar

Division of Gastrointestinal and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands.

Find articles by Ottenhoff, R. in: PubMed | Google Scholar

Division of Gastrointestinal and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands.

Find articles by Liefting, W. in: PubMed | Google Scholar

Division of Gastrointestinal and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands.

Find articles by de Haan, J. in: PubMed | Google Scholar

Division of Gastrointestinal and Liver Diseases, Academic Medical Center, Amsterdam, The Netherlands.

Find articles by Jansen, P. in: PubMed | Google Scholar

Published August 1, 1989 - More info

Published in Volume 84, Issue 2 on August 1, 1989
J Clin Invest. 1989;84(2):476–483. https://doi.org/10.1172/JCI114189.
© 1989 The American Society for Clinical Investigation
Published August 1, 1989 - Version history
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Abstract

TR- mutant rats have an autosomal recessive mutation that is expressed as a severely impaired hepatobiliary secretion of organic anions like bilirubin-(di)glucuronide and dibromosulphthalein (DBSP). In this paper, the hepatobiliary transport of glutathione and a glutathione conjugate was studied in normal Wistar rats and TR- rats. It was shown that glutathione is virtually absent from the bile of TR- rats. In the isolated, perfused liver the secretion of glutathione and the glutathione conjugate, dinitrophenyl-glutathione (GS-DNP), from hepatocyte to bile is severely impaired, whereas the sinusoidal secretion from liver to blood is not affected. The secretion of GS-DNP was also studied in isolated hepatocytes. The secretion of GS-DNP from cells isolated from TR- rat liver was significantly slower than from normal hepatocytes. Efflux of GS-DNP was a saturable process with respect to intracellular GS-DNP concentration: Vmax and Km for efflux from TR- cells was 498 nmol/min.g dry wt and 3.3 mM, respectively, as compared with 1514 nmol/min.g dry wt and 0.92 mM in normal hepatocytes. These results suggest that the canalicular transport system for glutathione and glutathione conjugates is severely impaired in TR- rats, whereas sinusoidal efflux is unaffected. Because the defect also comes to expression in isolated hepatocytes, efflux of GS-DNP from normal hepatocytes must predominantly be mediated by the canalicular transport mechanism, which is deficient in TR- rats.

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