Iron In Your Eye

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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