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Blood, 1 July 2007, Vol. 110, No. 1, pp. 125-132. Prepublished online as a Blood First Edition Paper on March 21, 2007; DOI 10.1182/blood-2007-01-068148. This Article Full Text Full Text (PDF) Supplemental Figure and Videos All Versions of this Article: blood-2007-01-068148v1 110/1/125    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Sheftel, A. D. Articles by Ponka, P. Search for Related Content PubMed PubMed Citation Articles by Sheftel, A. D. Articles by Ponka, P. Related Collections Hematopoiesis and Stem Cells Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Direct interorganellar transfer of iron from endosome to mitochondrion Alex D. Sheftel1, An-Sheng Zhang2, Claire Brown3, Orian S. Shirihai4, and Prem Ponka1 1 Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital and Department of Physiology, McGill University, Montréal, QC; 2 Department of Cellular and Developmental Biology, Oregon Health & Science University, Portland, OR; 3 Life Science Complex Imaging Facility, McGill University, Montreal, QC; 4 Department of Pharmacology and Experimental Therapeutics, Tufts University, Boston, MA Iron is a transition metal whose physicochemical properties make it the focus of vital biologic processes in virtually all living organisms. Among numerous roles, iron is essential for oxygen transport, cellular respiration, and DNA synthesis. Paradoxically, the same characteristics that biochemistry exploits make iron a potentially lethal substance. In the presence of oxygen, ferrous iron (Fe2+) will catalyze the production of toxic hydroxyl radicals from hydrogen peroxide. In addition, Fe3+ is virtually insoluble at physiologic pH. To protect tissues from deleterious effects of Fe, mammalian physiology has evolved specialized mechanisms for extracellular, intercellular, and intracellular iron handling. Here we show that developing erythroid cells, which are taking up vast amounts of Fe, deliver the metal directly from transferrin-containing endosomes to mitochondria (the site of heme biosynthesis), bypassing the oxygen-rich cytosol. Besides describing a new means of intracellular transport, our finding is important for developing therapies for patients with iron loading disorders. 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[Abstract] [Full Text] [PDF] M. Whitnall, Y. S. Rahmanto, R. Sutak, X. Xu, E. M. Becker, M. R. Mikhael, P. Ponka, and D. R. Richardson The MCK mouse heart model of Friedreich's ataxia: Alterations in iron-regulated proteins and cardiac hypertrophy are limited by iron chelation PNAS, July 15, 2008; 105(28): 9757 - 9762. [Abstract] [Full Text] [PDF] M. Shvartsman, R. Kikkeri, A. Shanzer, and Z. I. Cabantchik Non-transferrin-bound iron reaches mitochondria by a chelator-inaccessible mechanism: biological and clinical implications Am J Physiol Cell Physiol, October 1, 2007; 293(4): C1383 - C1394. [Abstract] [Full Text] [PDF]

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