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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-03-0914. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-03-0914v1 102/1/357    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 Darbari, D. Articles by Kurantsin-Mills, J. Search for Related Content PubMed PubMed Citation Articles by Darbari, D. Articles by Kurantsin-Mills, J. Related Collections Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2003, Vol. 102, No. 1, pp. 357-364 RED CELLS Fluorescence measurements of the labile iron pool of sickle erythrocytes Deepika Darbari, Mark Loyevsky, Victor Gordeuk, John A. Kark, Oswaldo Castro, Sohail Rana, Victor Apprey, and Joseph Kurantsin-Mills From the Center for Sickle Cell Disease, the Department of Biophysics and Physiology, the Department of Pediatrics, the Department of Microbiology, the Department of Medicine, and the Statistical Genetics and Bioinformatics Unit, National Human Genome Center, Howard University College of Medicine and Howard University Hospital, Washington, DC. Sickle erythrocytes have increased ferritin and increased molecular iron on the inner membrane leaflet, and we postulated that cytosolic labile iron is also elevated. We used the fluorescent metal-losensor, calcein, and a permeant Fe2+ chelator to estimate labile cytoslic Fe2+, and calcein plus an Fe3+ chelator to estimate total cytosolic labile iron (Fe2+ + Fe3+). We measured membrane nonheme iron by its reactivity with ferrozine. As estimated by calcein and Fe2+ chelator, the mean ± SD labile Fe2+ concentration was significantly lower in hemoglobin (Hb) SS (n = 29) than hemoglobin AA (n = 17) erythrocytes (0.56 ± 0.35 µM versus 1.25 ± 0.65 µM; P < .001). In contrast, as estimated by calcein and Fe3+ chelator, total erythrocyte labile iron was similar in hemoglobin SS (n = 12) and hemoglobin AA (n = 10) participants (1.75 ± 0.41 µM versus 2.14 ± 0.93 µM; P = .2). Mean membrane nonheme iron levels were higher in hemoglobin SS cells than hemoglobin AA cells (0.0016 x 10-4 versus 0.0004 x 10-4 fmol/cell; P = .01), but much lower than the mean amounts of total labile iron (1.6-1.8 x 10-4 fmol/cell) or hemoglobin iron (18 000-19 000 x 10-4 fmol/cell). Both membrane iron and total labile iron were much less than the mean amount of iron potentially present in erythrocyte ferritin as calculated from results of other investigators (15 x 10-4 versus 34 x 10-4 fmol/cell in HbAA versus HbSS erythrocytes). We conclude that cytosolic labile iron is not elevated in hemoglobin SS erythrocytes and that elemental membrane iron is present in only trace amounts. (Blood. 2003;102:357-364) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. T. Jones, I. S. Trowbridge, and A. L. Harris Effects of transferrin receptor blockade on cancer cell proliferation and hypoxia-inducible factor function and their differential regulation by ascorbate. Cancer Res., March 1, 2006; 66(5): 2749 - 2756. [Abstract] [Full Text] [PDF]

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