Exogenous fructose 1,6-bisphosphate reduces K+ permeability in isolated rat hepatocytes
| Autor: | Jordi Bermúdez, Teresa Roig, Ramon Bartrons |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Cell Membrane Permeability Fructose 1 6-bisphosphate Membrane permeability Physiology Galactosamine Cell Separation Rats Sprague-Dawley chemistry.chemical_compound Downregulation and upregulation Internal medicine Fructosediphosphates medicine Animals Egtazic Acid Ion transporter Chelating Agents Drug Synergism Fructose Cell Biology Rubidium Rats medicine.anatomical_structure Endocrinology Liver chemistry Permeability (electromagnetism) Hepatocyte Potassium Biophysics Calcium Efflux |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1522-1563 0363-6143 |
| Popis: | The relationship between the protective effect of fructose 1,6-bisphosphate (F-1,6-P2) 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-P2 reduced metabolic activity without affecting the ATP content, which suggests a downregulation of the ATP turnover. Using 86Rb+ as a tracer, we analyzed the relationship between these metabolic changes and alterations in K+ fluxes. In the presence of F-1,6-P2 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-P2, 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-P2. 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-P2, as has been shown in the prevention of galactosamine-induced hepatotoxicity. |
| Databáze: | OpenAIRE |
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