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A. Amir, S. Dachir, L. Cohen, M. Cohen, H. Gutman, Y. Shalem, R. Brandeis, T. Kadar; The Pathological Mechanism of Delayed Injuries Following Sulfur Mustard Exposure: 2. A Correlation of Clinical Status With Growth Capacity of Epithelial Cells and Inflammatory Markers of the Cornea . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5004.
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© ARVO (1962-2015); The Authors (2016-present)
Ocular exposure to sulfur mustard (SM) vapor causes an acute lesion in all exposed rabbit eyes. Nevertheless, the typical delayed injury appears only in ∼50% of eyes. This work aimed to study whether the appearance of the delayed lesion could be correlated to impaired epithelium, and to ongoing inflammatory processes, thus indicating therapeutic strategies.
Animal Care and Use Committee approval at IIBR was obtained. Rabbit eyes were exposed to SM vapor and a clinical follow up was carried out for 1 month. Rabbits were euthanized and corneas processed for biochemical analyses and for primary corneal epithelial cell cultures from center (C) or periphery (P) of the corneas (ex vivo PRCEC). Proliferative capacity of epithelial cells was measured from cell yield of successful explants. Protein was measured by the Bradford method, CGRP by ELISA of acetic acid extracted corneas and PGE by RIA.
At 1 month post exposure, neovascularization appeared in 50% of corneas, thus 2 corneal populations were evident: non–impaired and impaired. In ex vivo PRCEC prepared from exposed corneas the yield of cells from C of all exposed corneas was smaller than the yield from control corneas. The yield from C or P impaired explants correlated inversely and significantly with the degree of impairment (p<0.05, 0.1<p<0.05 respectively). The yield from P non–impaired explants was similar to controls. However the yield from P of impaired explants was higher than controls indicating uncontrolled growth in impaired corneal epithelial cells. SM exposed corneas were 20% heavier than controls (p<0.005), and impaired corneas were 20% heavier than non– impaired (p<0.01). PGE content of corneas was 3 fold higher than controls (p<0.001), and impaired corneas had 50% higher PGE than non–impaired corneas (p<0.05). CGRP content was 5 fold higher in SM exposed corneas (p<0.001) but no significant difference was found between impaired and non–impaired corneas.
Impaired epithelial cell growth and persistent inflammation correlated with the clinical status of individual eyes during the delayed phase of the lesion. Such signs corroborate our suggestion that the pathological healing process and the ongoing inflammation in impaired eyes contribute to the delayed lesion. Our findings imply that supplement of growth factors and anti– inflammatory drugs during the delayed phase of the lesion might be beneficial.
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