ArticleToxicological sciences : an official journal of the Society of Toxicology2017
Histopathological and Molecular Changes in the Rabbit Cornea From Arsenical Vesicant Lewisite Exposure.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Unveiling the acute toxic pathology and transcriptomic signature of ocular exposure to phosgene oxime using an in vivo mouse model: A novel pilot study.Toxicology and applied pharmacology · 2025Article
- Chloropicrin induced ocular injury: Biomarkers, potential mechanisms, and treatments.Toxicology letters · 2024Review
- The Involvement of Unfolded Protein Response in the Mechanism of Nitrogen Mustard-Induced Ocular Toxicity.The Journal of pharmacology and experimental therapeutics · 2024Article
- Mouse Model of Nitrogen Mustard Ocular Surface Injury Characterization and Sphingolipid Signaling.International journal of molecular sciences · 2024Article
- Phenylarsine oxide induced corneal injury involves oxidative stress mediated unfolded protein response and ferroptotic cell death: Amelioration by NAC.Free radical biology & medicine · 2023Article
- Metabolomics for identifying pathways involved in vesicating agent lewisite-induced corneal injury.Experimental eye research · 2023Article
- Ocular injury progression and cornea histopathology from chloropicrin vapor exposure: Relevant clinical biomarkers in mice.Experimental eye research · 2023Article
- Cutaneous Exposure to Arsenicals Is Associated with Development of Constrictive Bronchiolitis in Mice.American journal of respiratory cell and molecular biology · 2023Article
- Research progress on animal models of corneal epithelial-stromal injury.International journal of ophthalmology · 2023Review
- Retinal injury mouse model and pathophysiological assessment of the effect of arsenical vesicants.Experimental eye research · 2023Article
- Effect of dexamethasone treatment at variable therapeutic windows in reversing nitrogen mustard-induced corneal injuries in rabbit ocular in vivo model.Toxicology and applied pharmacology · 2022Article
- Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.PloS one · 2021Article
- Ocular Surface - Merging Challenges and Opportunities.Translational vision science & technology · 2020Article
- Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals.Annals of the New York Academy of Sciences · 2020Article
- Cutaneous lewisite exposure causes acute lung injury.Annals of the New York Academy of Sciences · 2020Article
- Acute corneal injury in rabbits following nitrogen mustard ocular exposure.Experimental and molecular pathology · 2019Article
- Tissue-Derived Biological Particles Restore Cornea Properties in an Enzyme-Mediated Corneal Ectatic Model.Bioengineering (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Lewisite (LEW), a potent arsenical vesicating chemical warfare agent, poses a continuous risk of accidental exposure in addition to its feared use as a terrorist weapon. Ocular tissue is exquisitely sensitive to LEW and exposure can cause devastating corneal lesions. However, detailed pathogenesis of corneal injury and related mechanisms from LEW exposure that could help identify targeted therapies are not available. Using an established consistent and efficient exposure system, we evaluated the pathophysiology of the corneal injury in New Zealand white rabbits following LEW vapor exposure (at 0.2 mg/L dose) for 2.5 and 7.5 min, for up to 28 day post-exposure. LEW led to an increase in total corneal thickness starting at day 1 post-exposure and epithelial degradation starting at day 3 post-exposure, with maximal effect at day 7 postexposure followed by recovery at later time points. LEW also led to an increase in the number of blood vessels and inflammatory cells but a decrease in keratocytes with optimal effects at day 7 postexposure. A significant increase in epithelial-stromal separation was observed at days 7 and 14 post 7.5 min LEW exposure. LEW also caused an increase in the expression levels of cyclooxygenase-2, IL-8, vascular endothelial growth factor, and matrix metalloproteinase-9 at all the study time points indicating their involvement in LEW-induced inflammation, vesication, and neovascularization. The outcomes here provide valuable LEW-induced corneal injury endpoints at both lower and higher exposure durations in a relevant model system, which will be helpful to identify and screen therapies against LEW-induced corneal injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.