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Beneficial effects of topical anti-inflammatory drugs against sulfur mustard-induced ocular lesions in rabbits

TitleBeneficial effects of topical anti-inflammatory drugs against sulfur mustard-induced ocular lesions in rabbits
Publication TypeJournal Article
Year of Publication2000
AuthorsAmir A., Turetz J., Chapman S., Fishbeine E., Meshulam J., Sahar R., Liani H., Gilat E., Frishman G., Kadar T.
JournalJ Appl ToxicolJ Appl Toxicol
Volume20 Suppl 1
PaginationS109-114
Date PublishedDec
Accession Number11428620
KeywordsAnimals, Anti-Inflammatory Agents, Non-Steroidal/*pharmacology, Anti-Inflammatory Agents/*pharmacology, Cornea/pathology, Dermatologic Agents/*toxicity, Dexamethasone/*pharmacology, Diclofenac/*pharmacology, Eye Diseases/*chemically induced/*prevention & control, Eye/*drug effects/pathology, INFLAMMATION, Mustard Gas/*toxicity, Rabbits, Volatilization
Abstract

Ocular injuries following sulfur mustard (HD) exposure are characterized by an inflammatory response, observed as eyelid swelling, conjunctivitis, corneal oedema and cellular infiltration starting 1-4 h after exposure, depending on dose. These effects heal partially during the first 1-2 weeks after exposure, with the later appearance of neovascularization, recurrent erosions and recurrent oedema of the cornea (delayed response). We have shown previously that topically applied steroid treatment, administered after HD exposure, attenuated the extent of neovascularization, one of the characteristics of delayed ocular pathology in rabbits. The present study was designed to characterize further the initial inflammatory response and to elucidate the role of anti-inflammatory (AI) drugs as a potential therapy. Rabbit eyes were exposed to HD vapour (390 microg l(-1) for 2 min) and were treated with a topical commercial ophthalmic solution of dexamethasone or diclofenac, starting 1 h post-exposure (four times a day). Inflammation was evaluated by clinical observations, biochemical analysis of aqueous humour and by histology. Sulfur mustard exposure initiated typical clinical ocular symptoms within 4-6 h after exposure. Biochemical analysis of aqueous humour showed that protein content and prostaglandin E (PGE) increased significantly at 6 h and were still high 48 h after HD exposure. Light microscopy evaluation revealed severe damage to the cornea, characterized by epithelial denudation, oedema and cellular infiltration (mostly eosinophiles) in the stroma. Both treatments were effective in alleviating the clinical symptoms and in preventing the HD-induced increase in protein and PGE in the anterior chamber, as well as the cellular infiltration, in the corneal stroma. However, the AI treatments had no therapeutic effect on corneal erosions, and a short delay in epithelial regeneration was noted. It is concluded that AI drugs are potential candidates for the treatment of ocular lesions following HD exposure.

Short TitleJournal of applied toxicology : JAT

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