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Rajesh Agarwal, Dinesh G Goswami, Rama Kant, Ankita Nagvekar, Chapla Agarwal, Claire R croutch, Robert P Casillas, David A Ammar, J. Petrash, Neera Tewari-Singh; Ocular Injuries From Arsenical Vesicant Lewisite Exposure . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5824.
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Investigation of the clinical and histopathological progression of ocular injuries from arsenical vesicant lewisite [LEW; dichloro(2-chlorovinyl)arsine] exposure. LEW is a potential warfare and terrorist agent that causes severe ocular injury including edema of eyelids, inflammation, massive corneal necrosis, and blindness.
We evaluated the in vivo ocular injury in New Zealand white rabbit corneal tissues post-LEW (0.2 mg/L) vapor exposure for 2.5, 5.0, 7.5 and 10.0 min. Clinical assessment in terms of corneal opacity, ulceration and neovascularization, and conjunctival and iris injuries were scored. Histopathological and immunohistochemical studies in the rabbit cornea were carried out to study LEW-induced responses related to inflammation, cell death, vesication and neovascularization.
LEW-induced corneal opacity was observed starting at 6 h post-exposure, which maxed at 3 days post-exposure and started reducing thereafter. Corneal ulceration was observed in less than 25% of corneal surface from 6 h to 28 days post-exposure in all LEW vapor exposures. LEW also induced neovascularization starting at 3 days post-exposure, which peaked at 22-28 days post-exposure, and initiated an increase in the redness and swelling of the conjunctiva and redness in the iris by 6 h post-exposure. LEW exposure for 5 -10 min caused over 50% increase in cornel thickness at 3 days, indicating an inflammatory response. Similarly, at 3 days post- exposure, epithelial layer degradation and apoptotic cell death were observed, and a LEW dose-dependent keratocyte cell death and an increase in inflammatory cells in the stroma were also evident. At 28 days post-exposure, LEW-induced changes in epithelial layer, corneal thickness and apoptotic cell death were reduced; however, an increase in the number of inflammatory cells and blood vessels in the stroma was more pronounced.
These findings provide first evidence of clinical and histopathological sequelae of ocular injury from LEW vapor, which could help establish relevant study endpoints and animal model to further identify effective and targeted therapies against vesicant-induced corneal injuries.
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