Abstract
Iron is essential for life, while excess iron can be toxic. Iron generates hydroxyl radical, which is the most reactive free radical, causing oxidative stress. Since iron is absorbed through the diet but not excreted from the body, it accumulates with age in tissues, including the retina, consequently leading to age-related toxicity. This accumulation is further promoted by inflammation. Hereditary diseases such as aceruloplasminemia, Friedreich’s ataxia, pantothenate kinase-associated neurodegeneration, and posterior column ataxia with retinitis pigmentosa involve retinal degeneration associated with iron dysregulation. In addition to hereditary causes, dietary or parenteral iron supplementation has been recently reported to elevate iron levels in the retinal pigment epithelium (RPE) and promote retinal degeneration. Ocular siderosis from intraocular foreign bodies or subretinal hemorrhage can also lead to retinopathy. Evidence from mice and humans suggests that iron toxicity may contribute to age-related macular degeneration pathogenesis. Iron chelators can protect photoreceptors and RPE in various mouse models. The therapeutic potential for iron chelators is under investigation.
Highlights
RPE65 is an iron-dependent enzyme used by the retinal pigment epithelium (RPE) to catalyze the conversion of all-trans-retinyl ester to 11-cis-retinol, a critical step in the visual cycle [2,3]
Abnormal iron homeostasis in hereditary diseases ocular can lead to retinal overload and intraocular foreign body or from iron released from red blood cells after intraocular hemorrhage can degeneration
Recent evidence suggests thatred iron toxicity contribute to the pathogenesis intraocular foreign body or from iron released from blood cellscan after intraocular hemorrhage can of age-related macular degeneration
Summary
Iron must be tightly regulated to provide needed iron while shielding retinal cells from iron-induced oxidative damage. This regulation is provided in the retina by a series of iron handling proteins. Iron can be transported to Pharmaceuticals 2018, 11, 112; doi:10.3390/ph11040112 www.mdpi.com/journal/pharmaceuticals The iron can be exported from cells by the iron exporter ferroportin (Fpn), within cytosolic ferritin. The iron can be exported from cells by the iron exporter ferroportin (Fpn), working in the the ferroxidases ceruloplasmin (Cp) or(Cp) hephaestin (Hp). Divalent transporter-1; Fpn, ferroportin; Hp, hephaestin; Tf, transferrin; TfR, transferrin receptor.
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