Exogenous fructose 1,6-bisphosphate reduces K+ permeability in isolated rat hepatocytes

被引:26
作者
Roig, T
Bartrons, R
Bermudez, J
机构
[1] UNIV BARCELONA, FAC ODONTOL, UNITAT BIOFIS, E-08907 LHOSPITALET DE LLOBREGAT, SPAIN
[2] UNIV BARCELONA, FAC ODONTOL, UNITAT BIOQUIM, E-08907 LHOSPITALET DE LLOBREGAT, SPAIN
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1997年 / 273卷 / 02期
关键词
potassium channels; metabolic downregulation; channel arrest; galactosamine;
D O I
10.1152/ajpcell.1997.273.2.C473
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The relationship between the protective effect of fructose 1,6-bisphosphate (F-1,6-P-2) against cell injury and the modifications produced in the metabolic fluxes and in the membrane permeability to K+ was studied in isolated rat hepatocytes. Incubation of these cells in the presence of F-1,6-P-2 reduced metabolic activity without affecting the ATP content, which suggests a downregulation of the ATP turnover. Using Rb-86(+) as a tracer, we analyzed the relationship between these metabolic changes and alterations in K+ fluxes. In the presence of F-1,6-P-2 the passive and the active K+ fluxes in hepatocytes decreased. However, the Na+-K+ pump from semipurified membranes was not directly affected by F-1,6-P-2, which suggests a secondarily induced reduction of Na+-K+ pump activity. Moreover, galactosamine-treated cells showed a marked increase in permeability to K+ that was abolished by the presence of F-1,6-P-2. This protective effect may be related to the prevention of K+ efflux. The results reported here strongly suggest the induction of channel arrest, and the associated metabolic downregulation, as the primary protective effect of F-1,6-P-2, as has been shown in the prevention of galactosamine-induced hepatotoxicity.
引用
收藏
页码:C473 / C478
页数:6
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