May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Mustard-Induced Ocular Injury in a Rabbit Model
Author Affiliations & Notes
  • A. Obolensky
    Ophthalmology, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • E. Banin
    Ophthalmology, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • Y. Morad
    Ophthalmology, Assaf Harofeh Medical Center, Zrifin, Israel
  • E. Berenshtein
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • C. Yahalom
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • F. Adibelli
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • M. DeAnda
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • J. Pe’er
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • J. Frucht-Pery
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • M. Chevion
    Cellular Biochemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel
  • Footnotes
    Commercial Relationships  A. Obolensky, None; E. Banin, None; Y. Morad, None; E. Berenshtein, None; C. Yahalom, None; F. Adibelli, None; M. DeAnda, None; J. Pe’er, None; J. Frucht-Pery, None; M. Chevion, Hebrew University Issum P.
  • Footnotes
    Support  Israel Defense Forces Medical Corps and the Bergman Memorial Fund
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 3847. doi:
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      A. Obolensky, E. Banin, Y. Morad, E. Berenshtein, C. Yahalom, F. Adibelli, M. DeAnda, J. Pe’er, J. Frucht-Pery, M. Chevion; Mustard-Induced Ocular Injury in a Rabbit Model . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3847.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To characterize ocular injury following corneal exposure to Nitrogen Mustard (NM, mechlorethamine) in a rabbit model. Methods: Twenty-eight New Zealand Albino rabbits were used. To induce ocular injury, 1 or 2% NM was applied to the center of the cornea of one eye of each animal for 5 minutes within a trephine. Vigorous rinsing was then performed. Fellow eyes and eyes in which saline was similarly applied served as control. Examiners masked to the treatment groups assessed magnitude of ocular injury. Repeated slit-lamp examinations with scoring of anterior segment injury, measurements of intraocular pressure (IOP), color photos of anterior segment, fluorescein angiography (FA), electroretinography (ERG), and blood testing of anti-oxidant status were performed. At 4-8 weeks after NM injury, animals were sacrificed and eyes were enucleated for histological processing. Results: Early-on, corneal erosions and edema were evident in NM-exposed eyes, accompanied by conjunctival chemosis and injection. Dilation of iris vessels, iris stromal hemorrhages and an inflammatory anterior chamber reaction were present. IOP was elevated in all NM-injured eyes during the acute phase, peaking on day 4 after injury. Later, severe corneal scarring and neovascularization developed and in 4 out of 8 eyes exposed to 2% NM, corneal perforation occurred after 3-4 weeks. Iris pigmentation, atrophy and in some cases also cataract, became evident. Systemically, marked depletion of ascorbic acid was induced by NM exposure. ERG that was performed at 6-7 weeks post-injury showed retinal function was not affected. On histological examination, epidermalization of the corneal epithelium, severe inflammation within the corneal stroma, loss of iris ruggae and cataractous changes were seen. Conclusions: NM exposure leads to severe dose-dependent injury in ocular anterior segment structures. The reduction in ascorbic acid levels supports the notion that free radical formation plays a role in mediating NM-induced ocular injury. In view of the risk that mustard warfare agents could be deployed by terrorists or on the battlefield, better understanding of the mechanisms underlying their toxicity as well as improved treatment modalities are needed.

Keywords: animal model • anterior segment • oxidation/oxidative or free radical damage 
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