ArticleToxicology letters2011
Sulfur mustard analog, 2-chloroethyl ethyl sulfide-induced skin injury involves DNA damage and induction of inflammatory mediators, in part via oxidative stress, in SKH-1 hairless mouse skin.
Article in Toxicology letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- HSP90, a Common Therapeutic Target for Suppressing Skin Injury Caused by Exposure to Chemically Diverse Classes of Blistering Agents.The Journal of pharmacology and experimental therapeutics · 2024Article
- Methimazole, an Effective Neutralizing Agent of the Sulfur Mustard Derivative 2-Chloroethyl Ethyl Sulfide.ACS bio & med chem Au · 2023Article
- Article
- Phosgene oxime: a highly toxic urticant and emerging chemical threat.Toxicology mechanisms and methods · 2021Review
- Screening of the chemoprotective effect of 13 compounds and their mixtures with sodium 2-mercaptoethanesulfonate against 2-chloroethyl ethyl sulfide.Journal of applied biomedicine · 2019Article
- Phosgene oxime: Injury and associated mechanisms compared to vesicating agents sulfur mustard and lewisite.Toxicology letters · 2018Review
- TRPA1 and CGRP antagonists counteract vesicant-induced skin injury and inflammation.Toxicology letters · 2018Article
- Article
- Nitrogen mustard-induced corneal injury involves the sphingomyelin-ceramide pathway.The ocular surface · 2018Article
- From the Cover: Catalytic Antioxidant Rescue of Inhaled Sulfur Mustard Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Defining cutaneous molecular pathobiology of arsenicals using phenylarsine oxide as a prototype.Scientific reports · 2016Article
- Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy.Annals of the New York Academy of Sciences · 2016Review
- 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
- Article
- Nitrogen mustard exposure of murine skin induces DNA damage, oxidative stress and activation of MAPK/Akt-AP1 pathway leading to induction of inflammatory and proteolytic mediators.Toxicology letters · 2015Article
- Flavanone silibinin treatment attenuates nitrogen mustard-induced toxic effects in mouse skin.Toxicology and applied pharmacology · 2015Article
- Topical nitrogen mustard exposure causes systemic toxic effects in mice.Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie · 2015Article
- Catalytic antioxidant AEOL 10150 treatment ameliorates sulfur mustard analog 2-chloroethyl ethyl sulfide-associated cutaneous toxic effects.Free radical biology & medicine · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Bifunctional alkyalating agent, sulfur mustard (SM)-induced cutaneous injury is characterized by inflammation and delayed blistering. Our recent studies demonstrated that 2-chloroethyl ethyl sulfide (CEES), a monofunctional analog of SM that can be used in laboratory settings, induces oxidative stress. This could be the major cause of the activation of Akt/MAP kinase and AP1/NF-κB pathways that are linked to the inflammation and microvesication, and histopathological alterations in SKH-1 hairless mouse skin. To further establish a link between CEES-induced DNA damage and signaling pathways and inflammatory responses, skin samples from mice exposed to 2 mg or 4 mg CEES for 9-48 h were subjected to molecular analysis. Our results show a strong CEES-induced phosphorylation of H2A.X and an increase in cyclooxygenase-2 (COX-2), inducible NOS (iNOS), and matrix metalloproteinase-9 (MMP-9) levels, indicating the involvement of DNA damage and inflammation in CEES-induced skin injury in male and female mice. Since, our recent studies showed reduction in CEES-induced inflammatory responses by glutathione (GSH), we further assessed the role of oxidative stress in CEES-related DNA damage and the induction of inflammatory molecules. Oral GSH (300 mg/kg) administration 1h before CEES exposure attenuated the increase in both CEES-induced H2A.X phosphorylation (59%) as well as expression of COX-2 (68%), iNOS (53%) and MMP-9 (54%). Collectively, our results indicate that CEES-induced skin injury involves DNA damage and an induction of inflammatory mediators, at least in part via oxidative stress. This study could help in identifying countermeasures that alone or in combination, can target the unveiled pathways for reducing skin injury in humans by SM.
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