Redox active plasma iron in C282Y/C282Y hemochromatosis
Open accessAbstract
Labile plasma iron (LPI) represents the redox active component of non–transferrin-bound iron (NTBI). Its presence in thalassemic patients has been recently reported. The aim of the present study was to quantify LPI in HFE genetic hemochromatosis (GH) and to characterize the mechanisms accounting for its appearance. We studied 159 subjects subdivided into the following groups: (1) 23 with iron overloaded GH; (2) 14 with iron-depleted GH; (3) 26 with dysmetabolic hepatosiderosis; (4) 33 with alcoholic cirrhosis; (5) 63 healthy controls. Both NTBI and LPI were substantially higher in patients with iron-overloaded GH than in those with iron-depleted GH or in healthy controls. LPI was significantly correlated with serum transaminase increase in this group. LPI was elevated in the alcoholic cirrhosis subgroup of severely affected patients. LPI was found essentially when transferrin saturation exceeded 75%, regardless of the etiologic condition. Transferrin saturation above 75% was related to iron overload in GH and to liver failure in alcoholic cirrhosis. LPI is present in C282Y/C282Y hemochromatosis and may be a marker of toxicity due to its potential for catalyzing the generation of reactive oxygen radicals in vivo.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Mutations in genes of the hepcidin-ferroportin axis disrupt iron homeostasis, leading to increased iron absorption, high transferrin saturation and increased toxicity from non-transferrin bound iron (NTBI) species.
“Mutations in genes of the hepcidin-ferroportin axis disrupt iron homeostasis, leading to increased iron absorption, high transferrin saturation and increased toxicity from non-transferrin bound iron (NTBI) species.78”
From Iron metabolism and iron disorders revisited in the hepcidin era (2020) · cites this paper as [78]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 28 · Cited by 151
- Authors
- Le Lan, C., Loréal, O., Cohen, T., Ropert, M., Glickstein, H., Lainé, F., Pouchard, M., Deugnier, Y., Le Treut, A., Breuer, W., Cabantchik, Z. I., & Brissot, P.
- Affiliations
- From the Service des Maladies du Foie and INSERM U-522 and the Laboratoire de Biochimie Générale et Enzymologie, University Hospital Pontchaillou, and the Centre d'examen de Santé CPAM, Rennes, France; and the Department of Biological Chemistry, Institute of Life Sciences, Hebrew University of Jerusalem, Israel.
- Inserm (FR)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2005-06-01
- Volume
- 105
- Issue
- 11
- Pages
- 4527-4531
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2142792785
- Cited by
- 151
- References
- 28
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 9 · 2022: 12 · 2021: 7 · 2020: 9 · 2019: 2 · 2018: 8 · 2017: 9 · 2016: 11 · 2015: 6 · 2014: 9 · 2013: 6 · 2012: 6
- FWCI
- 3.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Keywords
- labile plasma iron, non-transferrin-bound iron, HFE hemochromatosis, iron overload, iron depletion, alcoholic cirrhosis, transferrin saturation, liver failure, reactive oxygen species
- MeSH terms
- Hemochromatosis Protein, Iron Deficiencies, Adult, Transaminases, Genotype, Hemochromatosis, Humans, Iron, Liver Cirrhosis, Alcoholic, Male, Membrane Proteins, Middle Aged, Oxidation-Reduction, Prospective Studies, Transferrin, Histocompatibility Antigens Class I, Case-Control Studies, Iron Overload, Mutation, Missense
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review