Galzigna L, Rizzoli V, Bianchi M, Rigobello M P, Scuri R
Institute of Biological Chemistry, University of Padova, Italy.
Cell Biochem Funct. 1989 Apr;7(2):91-6. doi: 10.1002/cbf.290070203.
This study aims at elucidating the mechanism of action of extracellular fructose-1,6-diphosphate (FDP). FDP is able to inhibit Ca++ entry into the myocardial tissue with an IC50 value of 11.5 mM and in addition, it is bound by rat heart slices, the binding being activated by Zn and conditions of chemical hypoxia induced by KCN and iodoacetate. The overall effect of extracellular FDP includes an increase of frequency and amplitude of contraction of perfused heart at concentration below 1 mM, and, in general, a stimulation of the oxygen consumption of the tissue. The antihaemolytic effect of FDP suggests its action as a membrane stabilizer. The effects of extracellular FDP on the myocardial cell can be interpreted both on the basis of a limited permeability of the cell membrane to it and as a purely extracellular effect transduced through the cell membrane with a final response consisting of an increase in the intracellular FDP.
本研究旨在阐明细胞外1,6 -二磷酸果糖（FDP）的作用机制。FDP能够抑制Ca++进入心肌组织，其半数抑制浓度（IC50）值为11.5 mM，此外，大鼠心脏切片能结合FDP，锌以及由氰化钾和碘乙酸诱导的化学性缺氧条件可激活这种结合。细胞外FDP的总体作用包括在浓度低于1 mM时增加灌注心脏的收缩频率和幅度，并且总体上刺激组织的耗氧量。FDP的抗溶血作用表明其作为膜稳定剂的作用。细胞外FDP对心肌细胞的作用既可以基于细胞膜对其有限的通透性来解释，也可以解释为通过细胞膜转导的纯粹细胞外效应，最终反应是细胞内FDP增加。
