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The driving force for efflux of dinitrophenyl-glutathione (GS-DNP) and oxidized glutathione (GSSG) from freshly isolated rat hepatocytes was studied. Incubation of hepatocytes in Krebs with increasing K+ concentrations (equivalently replaced for Na+) or in Krebs with 3 mM ouabain led to a partial or complete dissipation of the plasma membrane potential, as measured by the equilibrium distribution of 36Cl-. This had no effect on the initial efflux rate of GSSG and GS-DNP. On the other hand, partial depletion of the cellular ATP content via different independent mechanisms significantly reduced the initial efflux rate of these compounds. Titration of the cellular ATP content by incubation of the cells with different concentrations of atractyloside revealed a linear relation between the cellular ATP content and the initial efflux rate of GS-DNP. The efflux of GS-DNP was also studied in hepatocytes from mutant rats with hepatobiliary transport defect (TR- rats). These rats have a hereditary canalicular secretion defect for a number of organic anions including GS-DNP. As we have shown previously, the efflux of GS-DNP from TR- rat hepatocytes is significantly slower than from normal hepatocytes (J. Clin. Invest. 84: 476-483, 1989). Depletion of the cellular ATP content in these cells had no significant effect on the residual efflux of GS-DNP. From these studies, we conclude that an ATP-dependent transport system for oxidized glutathione and glutathione conjugates is involved in the biliary transport of these compounds. The possible relation of this transport system with that described in other cell types and tissues, like erythrocytes and heart sarcolemma, is discussed.
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
October 1988,
The American journal of physiology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
February 1986,
The American journal of physiology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
July 2001,
American journal of physiology. Gastrointestinal and liver physiology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
August 1984,
The Journal of biological chemistry,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
September 1986,
The American journal of physiology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
March 1988,
Biochemistry,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
January 1984,
Methods in enzymology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
June 1989,
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
January 1984,
The American journal of physiology,
R P Oude Elferink, and
R Ottenhoff, and
W G Liefting, and
B Schoemaker, and
A K Groen, and
P L Jansen
May 1990,
Hepatology (Baltimore, Md.),
