Characterization of glutathione efflux from Hep G2 cells.
Previous studies have suggested that both cAMP-dependent signal transduction pathway and Ca2+/protein kinase C-dependent pathway are involved in GSH efflux from hepatocytes. In the present study, GSH efflux from Hep G2 cells, a human-derived hepatoma cell line, was further characterized. Both epidermal growth factor (0.1-10 ng/ml) and insulin (1 microgram/ml) significantly increased GSH efflux from Hep G2 cells. A fall in the membrane potential produced by the replacement of Na+ with equivalent K+ did not affect GSH efflux significantly. Neither ouabain, a Na+/K+ ATPase inhibitor, vanadate, a Ca2+ ATPase inhibitor, nor BaCl2, a K+ channel blocker, significantly affected the GSH efflux. Methionine (1mM) decreased GSH efflux from the cells, although total GSH content in the cells was not affected during the incubation time of 60 min. Signal transductions through tyrosine kinase-coupled receptors may also be involved in GSH efflux from hepatocytes.
Liu
J H
JH
Division of Health Science, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
Miyakawa
H
H
Liu
J
J
Mori
K
K
Takano
T
T
Marumo
F
F
Sato
C
C
D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D006528:Carcinoma, Hepatocellular / Q000188:drug therapy / Q000378:metabolism*; D002460:Cell Line; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005978:Glutathione / Q000096:biosynthesis*; D006801:Humans; D007328:Insulin / Q000494:pharmacology; D008113:Liver Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D008715:Methionine / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects; D020794:Receptor Protein-Tyrosine Kinases / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D014407:Tumor Cells, Cultured
D007328:Insulin; D015221:Potassium Channels; D004815:Epidermal Growth Factor; D008715:Methionine; D020794:Receptor Protein-Tyrosine Kinases; D000251:Adenosine Triphosphatases; D005978:Glutathione