Zinc may protect remote ocular injury caused by intestinal ischemia reperfusion in rats.

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.