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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4527-4531. Prepublished online as a Blood First Edition Paper on January 25, 2005; DOI 10.1182/blood-2004-09-3468. This Article Full Text (PDF) All Versions of this Article: 2004-09-3468v1 105/11/4527    most recent Alert me when this article is cited Alert me if a correction is posted 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 Le Lan, C. Articles by Brissot, P. Search for Related Content PubMed PubMed Citation Articles by Le Lan, C. Articles by Brissot, P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 13, 2004 Accepted January 13, 2005 Redox active plasma iron in C282Y/C282Y hemochromatosis Caroline Le Lan, Olivier Loreal, Tally Cohen, Martine Ropert, Hava Glickstein, Fabrice Laine, Michel Pouchard, Yves Deugnier, Andre Le Treut, William Breuer, Z I Cabantchik, and Pierre Brissot* Service des Maladies du Foie and INSERM U-522, University Hospital Pontchaillou, Rennes, France Department of Biological Chemistry, Institute of Life Sciences, Hebrew University of Jerusalem, Jerusalem, Israel Laboratoire de Biochimie Generale et Enzymologie, University Hospital Pontchaillou, Rennes, France Centre d'examen de Sante, CPAM, Rennes, France * Corresponding author; email: pierre.brissot{at}univ-rennes1.fr. Labile Plasma Iron (LPI) represents the redox active component of Non-Transferrin-Bound Iron (NTBI). Its presence in thalassemic patients has been recently reported (Esposito, Blood, 2003). The aim of the present study was to quantify LPI in HFE-1 Genetic Hemochromatosis (GH) and to characterize the mechanisms accounting for its appearance. We studied 159 subjects subdivided into: i) 23 iron overloaded GH; ii) 14 iron-depleted GH; iii) 26 Dysmetabolic hepatosiderosis; iv) 33 Alcoholic cirrhosis; v) 63 Normal controls. Results: (i): Both NTBI and LPI were substantially higher in iron overloaded GH than in iron depleted GH or normal controls. (ii) LPI was significantly correlated with serum transaminase increase in this group. (iii) LPI was elevated in the alcoholic cirrhosis subgroup of severely affected patients. iv) LPI was found essentially when transferrin saturation exceeded 75%, regardless of the etiological condition. v) Transferrin saturation above 75% was related to iron overload in GH and to liver failure in alcoholic cirrhosis. Conclusions: LPI is present in C282Y/C282Y hemochromatosis and may be a marker of toxicity due to its potential for catalysing the generation of reactive oxygen radicals in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D.-H. Lee, D. Y. Liu, D. R. Jacobs Jr., H.-R. Shin, K. Song, I.-K. Lee, B. Kim, and R. C. Hider Common Presence of Non-Transferrin-Bound Iron Among Patients With Type 2 Diabetes Diabetes Care, May 1, 2006; 29(5): 1090 - 1095. [Abstract] [Full Text] [PDF] P. Brissot and F. de Bels Current Approaches to the Management of Hemochromatosis Hematology, January 1, 2006; 2006(1): 36 - 41. [Abstract] [Full Text] [PDF]

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