ArticleExperimental and molecular pathology2019
Acute corneal injury in rabbits following nitrogen mustard ocular exposure.
Article in Experimental and molecular pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- BRD4 inhibition mitigates acute and chronic corneal injury following topical nitrogen mustard exposure.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Dexamethasone alters the cornea transcriptome to confer protection against ocular sulfur mustard exposure via regulating NFκB and TGFβ signaling in an in vivo rabbit model.Archives of toxicology · 2026Article
- Nitrogen mustard causes progressive tissue injury, severe DNA damage, and necroptosis in the cornea.Experimental eye research · 2025Article
- 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
- Article
- A novel therapy to ameliorate nitrogen mustard-induced limbal stem cell deficiency using lipoprotein-like nanoparticles.NPJ Regenerative medicine · 2025Article
- Article
- Activation of limbal epithelial proliferation is partly controlled by the ACE2-LCN2 pathway.iScience · 2024Article
- Dexamethasone sodium phosphate loaded nanoparticles for prevention of nitrogen mustard induced corneal injury.Experimental eye research · 2024Article
- Nitrogen Mustard-Induced Ex Vivo Human Cornea Injury Model and Therapeutic Intervention by Dexamethasone.The Journal of pharmacology and experimental therapeutics · 2024Article
- Establishing a Dexamethasone Treatment Regimen To Alleviate Sulfur Mustard-Induced Corneal Injuries in a Rabbit Model.The Journal of pharmacology and experimental therapeutics · 2024Article
- 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
- Insights into mustard gas keratopathy- characterizing corneal layer-specific changes in mice exposed to nitrogen mustard.Experimental eye research · 2023Article
- Cellular senescence implication in mustard keratopathy.Experimental eye research · 2023Article
- A corneo-retinal hypercitrullination axis underlies ocular injury to nitrogen mustard.Experimental eye research · 2023Article
- Ocular injury progression and cornea histopathology from chloropicrin vapor exposure: Relevant clinical biomarkers in mice.Experimental eye research · 2023Article
- Dysregulation of the mTOR pathway by mechlorethamine.Toxicology · 2023Article
- Retinal injury mouse model and pathophysiological assessment of the effect of arsenical vesicants.Experimental eye research · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Sulfur mustard (SM), a potent vesicating chemical warfare agent, and its analog nitrogen mustard (NM), are both strong bi-functional alkylating agents. Eyes, skin, and the respiratory system are the main targets of SM and NM exposure; however, ocular tissue is most sensitive, resulting in severe ocular injury. The mechanism of ocular injury from vesicating agents' exposure is not completely understood. To understand the injury mechanism from exposure to vesicating agents, NM has been previously employed in our toxicity studies on primary human corneal epithelial cells and ex vivo rabbit cornea organ culture model. In the current study, corneal toxicity from NM ocular exposure (1%) was analyzed for up to 28 days post-exposure in New Zealand White male rabbits to develop an acute corneal injury model. NM exposure led to conjunctival and eyelid swelling within a few hours after exposure, in addition to significant corneal opacity and ulceration. An increase in total corneal thickness and epithelial degradation was observed starting at day 3 post-NM exposure, which was maximal at day 14 post-exposure and did not resolve until 28 days post-exposure. There was an NM-induced increase in the number of blood vessels and inflammatory cells, and a decrease in keratocytes in the corneal stroma. NM exposure resulted in increased expression levels of cyclooxygenase-2, Interleukin-8, vascular endothelial growth factor and Matrix Metalloproteinase 9 indicating their involvement in NM-induced corneal injury. These clinical, biological, and molecular markers could be useful for the evaluation of acute corneal injury and to screen for therapies against NM- and SM-induced ocular injury.
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