Chelator-mediated iron efflux from reticulocytes

摘要: The mechanism by which bipyridine and phenanthroline types of iron chelator inhibit uptake from transferrin efflux mediated pyridoxal isonicotinoyl hydrazone was investigated using rabbit reticulocytes with the aim providing more information on normal process developing erythroid cells. It shown that chelators block cellular chelating immediately after release while it is still in membrane fraction iron-chelator then released cells a very similar to respect kinetics sensitivity incubation temperature effects metabolic inhibitors other chemical reagents. These results are compatible conclusion both iron-chelators mainly present endocytotic vesicles exocytosis. were also hydrazone-mediated had taken up presence isoniazid, an inhibitor haem synthesis, cytosol mitochondria. In this case, complexes not Measurement diethyl ether/water partition coefficients 1,10-phenanthroline their gave much higher values for free chelators, supporting concept trap intracellularly because differences lipid solubility and, hence, permeability complexes.