Characterization of vasopressin-mediated GSH efflux from Hep G2 cells: significance of protein kinase C.
Vasopressin stimulated GSH efflux from Hep G2 cells. The maximal effect was observed at 10nM. Pretreatment with pertussis toxin or cholera toxin for 18 hr increased GSH efflux. Vasopressin-mediated GSH efflux was observed even in the cells pretreated with those compounds. Dibutyryl-cAMP or dibutyryl-cGMP enhanced GSH efflux although an additive effect of vasopressin was not observed. Glucagon and a phorbol ester independently increased GSH efflux while both compounds decreased the effect of vasopressin. Staurosporine, an inhibitor of protein kinase C, inhibited vasopressin-mediated GSH efflux. The effect of vasopressin was observed even in the absence of extracellular Ca2+. Vasopressin stimulates GSH efflux from Hep G2 cells and protein kinase C-dependent pathway may play a significant role in vasopressin-mediated GSH efflux.
Liu
J H
JH
Department of Public Health and Environmental Sciences, Faculty of Medicine, Tokyo Medical and Dental University, Japan.
Sato
C
C
Takano
T
T
Marumo
F
F
D000470:Alkaloids / Q000494:pharmacology; D001127:Arginine Vasopressin / Q000502:physiology*; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D008099:Liver / Q000166:cytology / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019311:Staurosporine; D014407:Tumor Cells, Cultured
D000470:Alkaloids; D001127:Arginine Vasopressin; D011493:Protein Kinase C; D005978:Glutathione; D019311:Staurosporine