Iron Overload In The Eye

Discussion in 'Optometry Archives' started by ironjustice, Mar 18, 2010.

  1. ironjustice

    ironjustice Guest

    Iron, the retina and the lens: A focused review.
    Exp Eye Res. 2010 Mar 12.
    García-Castiñeiras S.
    Dept. Ophthalmology, room A-912/914, School of Medicine,
    Medical Sciences Campus Bldg., 9(th) floor, Medical Center Area,
    RioPiedras, PR 00935; Dept. Ophthalmology, School of Medicine,
    PO Box 365067, San Juan, PR 00936-5067.

    This review is focused on iron metabolism in the retina and in
    the lens and its relation to their respective age-related
    pathologies, macular degeneration (AMD) and cataract (ARC).
    Several aspects of iron homeostasis are considered first in the
    retina and second in the lens, paying particular attention to
    the transport of iron through the blood-retinal barrier and through
    the lens epithelial cell barrier, to the immunochemistry of
    iron-related proteins and their expression in both the retina and the
    lens, and to the nature of the photochemical damage caused by UV
    light
    on both tissues.
    A comparative overview of some iron related parameters (total iron,
    transferrin (Tf), transferrin saturation and total iron binding
    capacity),
    in plasma and ocular tissues and fluids of three animal species is
    also
    presented.
    Based on results selected from the literature reviewed, and our own
    results, a scheme for the overall circulation of iron within and out
    of the
    eye is proposed, in which,
    (i) iron is pumped from the retina to the vitreous body by a
    ferroportin/ferroxidase-mediated process at the endfeet of Müller
    cells,
    (ii) vitreal Tf binds this iron and the complex diffuses towards the
    lens,
    (iii) the iron/Tf complex is incorporated into the lens extracellular
    space
    probably at the lens equator and moves to the epithelial-fiber
    interface,
    (iv) upon interaction with Tf receptors of the apical pole of lens
    epithelial
    cells, the iron/Tf complex is endocytosed and iron is exported as Fe3+
    by a
    ferroportin/ferroxidase-mediated process taking place at the basal
    pole of
    the epithelial cells, and
    (v) Fe3+ is bound to aqueous humor Tf and drained with the aqueous
    humor into
    systemic blood circulation for recycling.
    The proposed scheme represents an example of close cooperation between
    the
    retina and the lens to maintain a constant flow of iron within the eye
    that
    provides an adequate supply of iron to ocular tissues and secures the
    systemic
    recycling of this element.
    It does not discount the existence of additional ways for iron to
    leave the eye
    through the blood-retinal barrier.
    In this review both AMD and ARC are recognized as multifactorial
    diseases with
    an important photoxidative component, and exhibiting a remarkable
    similitude of
    altered local iron metabolism.
    The epidemiological relationship between ARC and ferropenic anemia is
    explained
    on the basis that hepcidin, the hormone responsible for the anemia of
    chronic
    inflammation, could paradoxically cause intracellular iron overload in
    the lens
    by interfering with the proposed ferroportin/ferroxidasemediated
    export of iron
    at the basal side of the anterior lens epithelium.
    Other authors have suggested that a similar situation is created in
    the retina
    in the case of AMD.

    PMID: 20230820
    Copyright © 2010. Published by Elsevier Ltd.
    ----------------

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    ironjustice, Mar 18, 2010
    #1
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  2. ironjustice

    Ken Guest

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    Ken, Mar 18, 2010
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