Abstract
Oxidative stress has been implicated in several age-related eye diseases, including age-related macular degeneration, glaucoma, and diabetic retinopathy, as well as in retinitis pigmentosa. Hahn et al1 have documented higher iron levels in eyes of patients with age-related macular degeneration than in eyes of age-matched controls (particularly chelatable iron deposition in the retinal pigment epithelium and Bruch membrane). Because iron catalyzes the Fenton reaction (which produces hydroxyl radical), these results may mean that iron-mediated oxidative stress contributes to retinal degeneration in age-related macular degeneration. Furthermore, mice deficient in the ferroxidases ceruloplasmin and hephaestin accumulate iron in the retina and subsequently have retinal degeneration with features of age-related macular degeneration.2,3 In these mice, iron chelation with the orally absorbed and cell-permeant iron chelator deferiprone (Ferriprox) ameliorated oxidative stress and protected against iron overload–induced retinal degeneration.4