ArticleExperimental and molecular pathology2011
Structural changes in the skin of hairless mice following exposure to sulfur mustard correlate with inflammation and DNA damage.
Article in Experimental and molecular pathology, 2011. 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, 60 citations in OpenAlex.
- Dermal Exposure to Vesicating Nettle Agent Phosgene Oxime: Clinically Relevant Biomarkers and Skin Injury Progression in Murine Models.The Journal of pharmacology and experimental therapeutics · 2024Article
- Skin Models Used to Define Mechanisms of Action of Sulfur Mustard.Disaster medicine and public health preparedness · 2023Review
- Exposure to the immunomodulatory chemical triclosan differentially impacts immune cell populations in the skin of haired (BALB/c) and hairless (SKH1) mice.Toxicology reports · 2022Article
- Characterization of the rabbit conjunctiva: Effects of sulfur mustard.Experimental and molecular pathology · 2021Article
- Phosgene oxime: a highly toxic urticant and emerging chemical threat.Toxicology mechanisms and methods · 2021Review
- Expression of Laminin γ2 Proteolytic Fragments in Murine Skin Following Exposure to Sulfur Mustard.Anatomical record (Hoboken, N.J. : 2007) · 2020Article
- Expression of cytokines and chemokines in mouse skin treated with sulfur mustard.Toxicology and applied pharmacology · 2018Article
- Phosgene oxime: Injury and associated mechanisms compared to vesicating agents sulfur mustard and lewisite.Toxicology letters · 2018Review
- Sulfur mustard induced mast cell degranulation in mouse skin is inhibited by a novel anti-inflammatory and anticholinergic bifunctional prodrug.Toxicology letters · 2018Article
- Expression of Laminin 332 in Vesicant Skin Injury and Wound Repair.Clinical dermatology (Wilmington, Del.) · 2018Article
- Tissue injury and repair following cutaneous exposure of mice to sulfur mustard.Annals of the New York Academy of Sciences · 2016Review
- Mustard vesicants alter expression of the endocannabinoid system in mouse skin.Toxicology and applied pharmacology · 2016Article
- Mustard vesicating agent-induced toxicity in the skin tissue and silibinin as a potential countermeasure.Annals of the New York Academy of Sciences · 2016Review
- Mitigation of nitrogen mustard mediated skin injury by a novel indomethacin bifunctional prodrug.Experimental and molecular pathology · 2016Article
- Corneal toxicity induced by vesicating agents and effective treatment options.Annals of the New York Academy of Sciences · 2016Review
- Tannic acid mitigates the DMBA/croton oil-induced skin cancer progression in mice.Molecular and cellular biochemistry · 2015Article
- Therapeutic potential of a non-steroidal bifunctional anti-inflammatory and anti-cholinergic agent against skin injury induced by sulfur mustard.Toxicology and applied pharmacology · 2014Article
- Article
- Structural changes in hair follicles and sebaceous glands of hairless mice following exposure to sulfur mustard.Experimental and molecular pathology · 2014Article
- Histopathological and immunohistochemical evaluation of nitrogen mustard-induced cutaneous effects in SKH-1 hairless and C57BL/6 mice.Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie · 2014Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Sulfur mustard (SM, bis(2-chloroethyl)sulfide) is a bifunctional alkylating agent that causes dermal inflammation, edema and blistering. To investigate the pathogenesis of SM-induced injury, we used a vapor cup model which provides an occlusive environment in which SM is in constant contact with the skin. The dorsal skin of SKH-1 hairless mice was exposed to saturated SM vapor or air control. Histopathological changes, inflammatory markers and DNA damage were analyzed 1-14 days later. After 1 day, SM caused epidermal thinning, stratum corneum shedding, basal cell karyolysis, hemorrhage and macrophage and neutrophil accumulation in the dermis. Cleaved caspase-3 and phosphorylated histone 2A.X (phospho-H2A.X), markers of apoptosis and DNA damage, respectively, were increased whereas proliferating cell nuclear antigen (PCNA) was down-regulated after SM exposure. By 3 days, epithelial cell hypertrophy, edema, parakeratosis and loss of epidermal structures were noted. Enzymes generating pro-inflammatory mediators including myeloperoxidase and cyclooxygenase-2 were upregulated. After 7 days, keratin-10, a differentiation marker, was evident in the stratum corneum. This was associated with an underlying eschar, as neoepidermis began to migrate at the wound edges. Trichrome staining revealed increased collagen deposition in the dermis. PCNA expression in the epidermis was correlated with hyperplasia, hyperkeratosis, and parakeratosis. By 14 days, there was epidermal regeneration with extensive hyperplasia, and reduced expression of cleaved caspase-3, cyclooxygenase-2 and phospho-H2A.X. These findings are consistent with the pathophysiology of SM-induced skin injury in humans suggesting that the hairless mouse can be used to investigate the dermatoxicity of vesicants and the potential efficacy of countermeasures.
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