In the eye, the retina and RPE (retinal pigmented epithelium) are exposed to high levels of oxidative radicals generated by light exposure and high metabolic rate. Degeneration of these cells due to cumulative oxidative damage plays an important role in diseases like AMD (Age-related Macular Degeneration) and subsequent blindness. The underlying mechanisms of AMD remain unclear, and therefore extensive studies are needed to help combat the disease. We use sodium iodate, an oxidizing agent that preferentially degenerate RPE, to induce oxidative stress in young and old mice. DJ-1, Parkinson’s Disease (PD)-associated gene protects neurons from oxidative damages. High levels of DJ-1 were observed in RPE and photoreceptors of adult mice retina. DJ-1 loss results in age-related mild structural and physiological changes in retinas of DJ-1 knockout mice. Control (C57BL/6) and DJ-1 knockout 3- and 15- month-old mice were injected with 10mg/kg sodium iodate to gain insight into oxidative stress mechanisms in RPE and retina.Histological sections revealed that oxidative stress in DJ-1 knockout resulted in increased RPE and photoreceptor cells degeneration compared to controls. Gene expression analysis for antioxidant genes was carried out. The transcript levels of these genes were significantly upregulated in RPE of DJ-1 knockout compared to control but downregulated in the retina in 3-month-old mice. In 15-month-old mice, transcript levels of these genes were significantly downregulated in RPE of DJ-1 knockout compared to control but remained unchanged in the retina. Injection of mice with 10mg/Kg NaIO3 differentially regulated the expression of these transcripts in the RPE and retinas. Overall, our data suggest that loss of DJ-1 renders RPE and retina more susceptible to oxidative damage.