Characterization of acute and delayed ocular lesions induced by sulfur mustard in rabbits

Purpose. To establish an experimental model for sulfur mustard-induced acut e and delayed ocular lesions in rabbits. Methods. Rabbit eyes were exposed to sulfur mustard (HD) vapor (370, 420 mu g/l) for a period of two minutes. A three months follow-up study was carrie d out, based on the evaluation of clinical, biochemical and histological pa rameters. Results. HD exposure initiated typical clinical symptoms within 2-6 hrs, ch aracterized by eye closure, eyelid swelling, conjunctival hyperemia, cornea l erosions and inflammation. The clinical signs were significantly dose-dep endent and reached a peak at 24-72 hrs post exposure. Biochemical evaluatio n of the aqueous humor exhibited an inflammatory reaction and oxidative str ess at 4 hrs after exposure, subsiding at 28 hrs after exposure. Histological examination of corneas at 48 hrs revealed epithelial denudatio n and marked stromal edema, accompanied by cellular infiltration. Epithelia l regeneration started after 72 hrs, and recovery was almost completed with in 1-2 weeks, depending on the HD dose. A second phase of pathological processes started as early as two weeks post exposure and was characterized by corneal edema, opacity, recurrent erosio ns and neovascularization. The delayed injuries were found in 25 and 40% of the eyes respectively, and when appearing, were more severe than the initi al ones. Conclusions. The development of HD-induced ocular lesions in rabbits is sim ilar to the lesions described in human casualties. Quantitative analysis of the various clinical parameters emphasizes the contribution of each tissue to the overall toxic picture. Our experimental model is useful for studyin g the pathological mechanisms of HD-ocular lesions, and may serve for testi ng potential therapies.