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Alterations in structure and density of corneal endothelium following sulfur mustard exposure in rabbits and its relation to long-term pathology

TitleAlterations in structure and density of corneal endothelium following sulfur mustard exposure in rabbits and its relation to long-term pathology
Publication TypeConference Proceedings
Year of Conference2008
AuthorsKadar T., Cohen M., Dachir S., Cohen L., Fishbine E., Sahar R., Amir A.
Conference NameProceedings of the U.S. Army Medical Defense Bioscience Review
Volume1, A129
Pagination162
Abstract

Sulfur mustard (SM) is an alkylating agent that induces cytotoxicity and sustained anterior segment inflammation. The present study aimed to investigate the response of corneal endothelium to chemical injury induced by sulfur mustard in rabbits and to elucidate its involvement in the development of long-term pathology. Rabbit eyes were exposed to SM vapor. A clinical followup, pachymetry for measurement of corneal thickness, and in vivo analysis of corneal endothelium using a contact specular microscope were carried out up to 3 months after exposure. The area and density of endothelial cells were calculated from digital photomicrographs taken by the contact specular microscope, utilizing a morphometric analysis (Image Pro). Animals were euthanized at different time points (1 hour-3 months), and eyes enucleated and processed for histology (using hemolysin-eosin staining, PAS, and TUNEL for apoptosis). SM induced acute corneal erosions and prolonged anterior segment inflammation. Corneal thickness increased within hours and declined after few days but still remained high in relation to the baseline value, indicating a chronic edema. Endothelial cell numbers declined significantly at 24-48 hours after exposure, due to apoptotic cell death observed by TUNEL staining. Although regeneration of the endothelium was relatively fast, the number of cells did not reach baseline values even 3 months after exposure. Moreover, histological evaluation of corneal sections revealed deformation and enlargement of many cells (polyploidy and multinucleated giant cells) and thickening of the Descemet membrane. These changes appeared more frequently in corneas displaying delayed pathology. We concude that SM-induced apoptotic cell death in the endothelium is associated with corneal edema. The impaired healing and the decrease in endothelial cell density may contribute to the development of delayed injuries. Because human corneal endotheliium is almost amitotic, endothelium toxicity should be taken into consideration when testing potential treatments against ocular injuries after SM exposure.

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