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  11. Unveiling The Acute Toxic Pathology And Transcriptomic Signature Of Ocular Exposure To Phosgene Oxime Using An In Vivo Mouse Model: A Novel Pilot Study

Unveiling the acute toxic pathology and transcriptomic signature of ocular exposure to phosgene oxime using an in vivo mouse model: A novel pilot study

Ebenezar Okoyeocha1, Natalie Vredevoogd1, Shreya Paithankar1

  • 1Department of Pharmacology and Toxicology, College of Osteopathic Medicine, Michigan State University, East Lansing, MI, USA.

Toxicology and Applied Pharmacology
|June 12, 2025

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View abstract on PubMed

Summary
This summary is machine-generated.

Phosgene oxime (CX) causes significant ocular damage, including corneal and retinal injury. This study identified key gene expression changes related to inflammation and cell death following CX exposure in mouse eyes.

Area of Science:

  • Ocular toxicology
  • Chemical warfare agents
  • Gene expression analysis

Background:

  • Phosgene oxime (CX) is a dangerous vesicant and potential chemical threat agent.
  • Ocular exposure to CX causes immediate tissue damage, but research on its specific effects and mechanisms is limited.
  • The eye is highly sensitive to chemical exposures, necessitating research into CX-induced ocular injuries.

Purpose of the Study:

  • To investigate the toxic pathophysiological effects of phosgene oxime (CX) exposure on mouse ocular tissue.
  • To identify molecular mechanisms underlying CX-induced ocular injuries.
  • To establish a foundation for developing CX-induced ocular injury models and identifying biomarkers.

Main Methods:

  • C57BL/6 mouse eyeballs were exposed to CX (15 or 30 seconds) or sham-treated.
Keywords:
Chemical warfare agentInjury biomarkersOcular chemical exposureOcular injury model

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  • Ocular tissues were collected 24 hours post-exposure for histological and RNA sequencing analysis.
  • Gene expression data were analyzed using DESeq2, with pathway enrichment performed via KEGG.

    • Main Results:

    • CX exposure led to significant corneal epithelial degradation, stromal cellularity increase, endothelial cell loss, and damage to the ciliary body, lens, and retina.
    • RNA sequencing identified 697 downregulated and 233 upregulated genes following ocular CX exposure (p≤0.01, |log2FC|≥1).
    • Pathway analysis revealed significant upregulation of inflammation (cytokines) and cell death (ferroptosis) pathways, and downregulation of metabolism and tight junction pathways.

    Conclusions:

    • Phosgene oxime (CX) induces severe, multi-tissue damage in the mouse eye.
    • CX exposure significantly alters gene expression, promoting inflammatory and cell death pathways while suppressing metabolic and structural pathways.
    • This study provides critical insights into CX ocular toxicity mechanisms, paving the way for future research on injury models, biomarkers, and therapeutic strategies.
    Phosgene oxime