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Remote organ injury represents the oxidative damage, which occurs in various organs away from the tissues exposed to ischemia-reperfusion insult. Hypothesizing that the eye may be susceptible to this type of tissue damage, we investigated the effect of splanchnic ischemia-reperfusion on the chorio-retinal tissue in Sprague-Dawley rats. Four groups, each consisting of 10 male rats, were designed for the study. Ischemia-reperfusion was introduced by clamping superior mesenteric artery for 1 hour, followed by reperfusion for 90 min (IR group). In another group, the same operation was performed except that zinc aspartate (50 mg/kg) was given intra-peritoneally 15 min before the opening of the clamp (Zn-IR group). As control (sham group), the abdomen was opened without any intervention on superior mesenteric artery. The other group was given Zn after opening of abdomen without any intervention on superior mesenteric artery (Zn-sham group). After the choroid and the retina were dissected from the eye, malondialdehyde, superoxide dismutase, catalase and nitric oxide (NO) were measured in the collected eye tissues. We found that the levels of malondialdehyde, an indicator for lipid peroxidation, were higher in the chorio-retinal tissue of IR group compared to Zn-IR, Zn-sham or sham group (p < 0.05). The oxidative stress in Zn-IR group was not higher than that of sham group. Treatment with zinc decreased NO levels but had no noticeable effect on the level of antioxidant enzymes. Our study indicates that remote organ injury is induced in the eye during splanchnic ischemia-reperfusion and that zinc may be beneficial to ameliorate remote ocular injury.remote ocular injury; zinc; IR injury; chorio-retinal oxidation

Purpose To evaluate the role of melatonin, an antioxidant agent, in diabetic oxidative stress and vascular damage. Methods Diabetes was induced in 21 male Wistar rats by intraperitoneal (IP) administration of streptozotocin and then the rats were equally and randomly allocated to diabetic, melatonin, and vehicle groups. Seven healthy normal rats with similar features comprised the control group as the fourth group. All animals were followed for 12 weeks. The melatonin group received IP melatonin daily and the vehicle group received 2.5% ethanol IP at the last month. At the end of 12 weeks, the rats were killed and retinas were harvested. The retinas were investigated for the existence of hypoxiainducible factor 1-a (HIF-1a), vascular endothelial growth factor A (VEGF-A), and pigment epithelium-derived factor (PEDF) by ELISA. Retinal oxidative stress is quantitated by measuring nitrotyrosine and malondialdehyde levels. Retinal immunohistochemistry with antibody against CD31 antigen was carried out on retinal cross-sections. For statistics, ANOVA test was used for multiple comparisons. Results Hyperglycemia increased retinal oxidation as measured through levels of nitrotyrosine and malondialdehyde. Diabetic retinas are also associated with abnormal vascular changes such as dilatation and deformation. HIF-1a, VEGF-A, and PEDF were all increased because of diabetic injury. Melatonin showed a potential beneficial effect on retinopathy in diabetic rats. It decreased retinal nitrotyrosine and malondialdehyde levels, showing an antioxidative support. The vasculomodulator cytokines are decreased accordingly by melatonin therapy. Melatonin normalized retinal vascular changes as well. ConclusionMelatonin may show some advantage on diabetic vascular changes through decreasing oxidative stress and vessel-related cytokines.

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Brimonidine and NAC supplementation provide antioxidative properties to retina and decrease retinal damage induced by ocular hypertension.