ferric-ammonium-citrate and ferric-chloride

Iron is an essential element for plant and animal life and is found in soil, fresh waters and marine waters. The Fe

Topics: Animals; Ferric Compounds; Invertebrates; Iron; Mammals; Neurons; Proprioception

Ferritin is the major intracellular iron storage protein which has been shown to protect cells against oxidative damage. Recent reports that an inherited abnormality in human ferritin synthesis is associated with early bilateral cataracts underscore the importance of understanding ferritin synthesis and iron storage in lens epithelial cells. We previously demonstrated that ascorbic acid greatly increases de novo synthesis of ferritin in lens epithelial cells. The objectives of the present study were to determine: (1) the effects of ascorbic acid and ferric ammonium citrate on iron uptake by canine lens epithelial cells from iron bound to transferrin and from ferric chloride and (2) the incorporation of this element into ferritin. Iron uptake by lens epithelial cells from 59ferric chloride was 20 times higher than from 59iron-transferrin and iron deposition into ferritin was 8-fold higher when 59ferric chloride was the source. Ascorbic acid had a stimulatory effect on iron uptake from transferrin and on incorporation of this element into ferritin. The ascorbic acid-induced increase of iron uptake required de novo protein synthesis but not specifically de novo ferritin biosynthesis. Although ferritin is not directly involved in iron uptake, the level of ferritin protein could control the pool of intracellular iron. The present results indicate that iron homeostasis in lens epithelial cells is affected mainly by changes in apoferritin synthesis, which is greatly stimulated by ascorbic acid, rather than by altering the rate of protein degradation, which is very slow in these cells under all circumstances. Ferric ammonium citrate activates iron uptake from transferrin in a wide range of cell lines by generation of free radicals. Ferric ammonium citrate also increased iron uptake from Tf in lens epithelial cells. Ferric ammonium citrate treated cells incorporated 5 times more iron and deposited 2 times more iron into ferritin than control cells. Increased incorporation of iron into ferritin was due to ferric ammonium citrate-induced stimulation of de novo ferritin synthesis rather than an increased rate of iron deposition into pre-existing ferritin. Ferric ammonium citrate had a different effect on iron uptake from ferric chloride; total iron uptake was not significantly increased while deposition into ferritin was significantly decreased. These results demonstrate that iron homeostasis in lens epithelial cells is regulated by ascorbic acid and by changes in th

Topics: Animals; Apoferritins; Ascorbic Acid; Cells, Cultured; Chlorides; Dogs; Epithelial Cells; Ferric Compounds; Homeostasis; Humans; Infant, Newborn; Iron Radioisotopes; Lens, Crystalline; Quaternary Ammonium Compounds; Transferrin

Iron participates in diverse pathologic processes by way of the Fenton reaction, which catalyzes the formation of reactive oxygen species (ROS). To test the hypothesis that this reaction accelerates apoptosis, we used human umbilical vein endothelial cells (HUVECs) as surrogates for the microvasculature in vivo.. HUVECs were loaded with Fe [III](ferric chloride and ferric ammonium citrate) with 8-hydroxyquinoline as carrier and were then challenged with two stimuli of the heat shock response, authentic heat or sodium arsenite. Iron dependence was tested with two chelators, membrane-impermeable deferoxamine and membrane-permeable o-phenanthroline. The role of ROS was assessed with superoxide dismutase, catalase, and the reporter compound dichlorofluorescein diacetate. The mechanism of cell death was assessed with three complementary techniques, Annexin V/propidium iodide labeling, the TUNEL stain, and electron microscopy.. Iron-loaded HUVECs executed apoptosis after a heat shock stimulus. Iron-catalyzed formation of ROS appeared to be a critical mechanism, because both chelation of iron and enzymatic detoxification of ROS attenuated this apoptosis.. Inorganic iron, in concert with chemical and physical inducers of the heat shock response, may trigger apoptosis. The accumulation of iron in injured tissue may thereby predispose to accelerated apoptosis and account, in part, for poor wound healing and organ failure.

Topics: Cell Survival; Cells, Cultured; Chlorides; Deferoxamine; Drug Carriers; Endothelium, Vascular; Ferric Compounds; Free Radicals; Hot Temperature; Humans; Iron Chelating Agents; Kinetics; Microcirculation; Models, Biological; Oxyquinoline; Phenanthrolines; Quaternary Ammonium Compounds; Reactive Oxygen Species; Umbilical Veins

The fungistatic capacity and serum ion levels (SI) of guinea pigs given subcutaneous injections of various iron solutions were examined. The administration of 2.0 ml of 0.1 M ferric ammonium sulfate, ferric sulfate, or ferric chloride subcutaneously had no significant effect on the SI 3 h after administration, whereas ferric ammonium citrate, ferric citrate, or ferrous sulfate elevated the SI to 50 to 140 times that necessary to saturate the unbound transferrin in normal sera. The sera from 11 of 15 guinea pigs with an elevated SI remained fungistatic for Trichophyton mentagrophytes, whereas 3 of 15 guinea pigs with an elevated SI remained fungistatic for Rhizopus oryzae. The sera from normal guinea pigs were consistently fungistatic for Rhizopus oryzae. The sera from normal guinea pigs were consistently fungistatic for both T. mentagrophytes and R. oryzae. These data suggest that subcutaneous administration of certain iron compounds can significantly elevate the SI without completely abolishing the fungistatic capacity of the serum.

Topics: Animals; Blood Physiological Phenomena; Chlorides; Ferric Compounds; Ferrous Compounds; Guinea Pigs; Iron; Quaternary Ammonium Compounds; Rhizopus; Trichophyton