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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