Many forms of retinal degeneration, including age-related macular degeneration (AMD), involve oxidative stress. Due to its multifactorial nature and because of the difference between humans and mice, murine models of AMD are limited. This is especially the case for geographic atrophy, a more advanced form of AMD. One way to model oxidative stress is through the systemic administration of sodium iodate (NaIO3). Herein, sex, age, and dose differences within the NaIO3 model are studied to provide researchers with a milder form of damage to allow therapeutics that would be protective in the more chronic AMD disease to also be protective in this acute model. Additionally, a novel model of inducing geographic atrophy using NaIO3 is described. One contributing factor of AMD and other oxidative stress diseases of the retina is iron toxicity. Many diseases and mouse models of iron toxicity suggest that iron is much more toxic in its ferrous state. To confirm this theory, hepcidin (Hepc) KO mice were used to induce iron overload, and in a subset of those mice the oxidant ceruloplasmin (Cp) was also knocked out. Cp/Hepc DKO mice had much more retinal toxicity than either single KO, demonstrating that ferrous iron is indeed more toxic than ferric iron. Overall, the work presented herein provide researchers with new ways of modeling oxidative stress in the retina and provide insights into new therapeutic approaches to treating oxidative stress and iron toxicity.