Iron In Your Eye

Discussion in 'Eye-Care' started by ironjustice, Oct 9, 2007.

  1. ironjustice

    ironjustice Guest

    Prog Retin Eye Res. 2007 Aug 11; [Epub ahead of print]
    Iron homeostasis and toxicity in retinal degeneration.He X, Hahn P,
    Iacovelli J, Wong R, King C, Bhisitkul R, Massaro-Giordano M, Dunaief
    JL.
    F.M. Kirby Center for Molecular Ophthalmology, Scheie Eye Institute,
    305 Stellar-Chance Labs, 422 Curie Boulevard, Philadelphia, PA 19104,
    USA.

    Iron is essential for many metabolic processes but can also cause
    damage. As a potent generator of hydroxyl radical, the most reactive
    of the free radicals, iron can cause considerable oxidative stress.
    Since iron is absorbed through diet but not excreted except through
    menstruation, total body iron levels buildup with age. Macular iron
    levels increase with age, in both men and women. This iron has the
    potential to contribute to retinal degeneration. Here we present an
    overview of the evidence suggesting that iron may contribute to
    retinal degenerations. Intraocular iron foreign bodies cause retinal
    degeneration. Retinal iron buildup resulting from hereditary iron
    homeostasis disorders aceruloplasminemia, Friedreich's ataxia, and
    panthothenate kinase-associated neurodegeneration cause retinal
    degeneration. Mice with targeted mutation of the iron exporter
    ceruloplasmin have age-dependent retinal iron overload and a resulting
    retinal degeneration with features of age-related macular degeneration
    (AMD). Post mortem retinas from patients with AMD have more iron and
    the iron carrier transferrin than age-matched controls. Over the past
    10 years much has been learned about the intricate network of proteins
    involved in iron handling. Many of these, including transferrin,
    transferrin receptor, divalent metal transporter-1, ferritin,
    ferroportin, ceruloplasmin, hephaestin, iron-regulatory protein, and
    histocompatibility leukocyte antigen class I-like protein involved in
    iron homeostasis (HFE) have been found in the retina. Some of these
    proteins have been found in the cornea and lens as well. Levels of the
    iron carrier transferrin are high in the aqueous and vitreous humors.
    The functions of these proteins in other tissues, combined with
    studies on cultured ocular tissues, genetically engineered mice, and
    eye exams on patients with hereditary iron diseases provide clues
    regarding their ocular functions. Iron may play a role in a broad
    range of ocular diseases, including glaucoma, cataract, AMD, and
    conditions causing intraocular hemorrhage. While iron deficiency must
    be prevented, the therapeutic potential of limiting iron-induced
    ocular oxidative damage is high. Systemic, local, or topical iron
    chelation with an expanding repertoire of drugs has clinical
    potential.

    PMID: 17921041 [PubMed - as supplied by publisher]


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    ironjustice, Oct 9, 2007
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