ArticleFree radical biology & medicine2014
Catalytic antioxidant AEOL 10150 treatment ameliorates sulfur mustard analog 2-chloroethyl ethyl sulfide-associated cutaneous toxic effects.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Oxidative Stress: An Intersection Between Radiation and Sulfur Mustard Lung Injury.Disaster medicine and public health preparedness · 2024Article
- Methimazole, an Effective Neutralizing Agent of the Sulfur Mustard Derivative 2-Chloroethyl Ethyl Sulfide.ACS bio & med chem Au · 2023Article
- The Use of Thiocyanate Formulations to Create Manganese Porphyrin Antioxidants That Supplement Innate Immunity.Antioxidants (Basel, Switzerland) · 2022Article
- HOxidative medicine and cellular longevity · 2021Review
- Antioxidant drug therapy as a neuroprotective countermeasure of nerve agent toxicity.Neurobiology of disease · 2020Review
- 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
- Mn Porphyrin-Based Redox-Active Drugs: Differential Effects as Cancer Therapeutics and Protectors of Normal Tissue Against Oxidative Injury.Antioxidants & redox signaling · 2018Review
- Expression of cytokines and chemokines in mouse skin treated with sulfur mustard.Toxicology and applied pharmacology · 2018Article
- Improvements in SOD mimic AEOL-10150, a potent broad-spectrum antioxidant.Military Medical Research · 2018Review
- Phosgene oxime: Injury and associated mechanisms compared to vesicating agents sulfur mustard and lewisite.Toxicology letters · 2018Review
- Scavenging reactive oxygen species inhibits status epilepticus-induced neuroinflammation.Experimental neurology · 2017Article
- 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
- Addressing the Symptoms or Fixing the Problem? Developing Countermeasures against Normal Tissue Radiation Injury.Radiation research · 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
- Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals.Biochemical pharmacology · 2016Review
- Reactive oxygen species mediate cognitive deficits in experimental temporal lobe epilepsy.Neurobiology of disease · 2015Article
- 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
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Our previous studies and other published reports on the chemical warfare agent sulfur mustard (SM) and its analog 2-chloroethyl ethyl sulfide (CEES) have indicated a role of oxidative stress in skin injuries caused by these vesicating agents. We examined the effects of the catalytic antioxidant AEOL 10150 in the attenuation of CEES-induced toxicity using our established skin injury models (skin epidermal cells and SKH-1 hairless mice) to validate the role of oxidative stress in the pathophysiology of mustard vesicating agents. Treatment of mouse epidermal JB6 and human HaCaT cells with AEOL 10150 (50μM) 1h post-CEES exposure resulted in significant (p < 0.05) reversal of CEES-induced decreases in both cell viability and DNA synthesis. Similarly, AEOL 10150 treatment 1h after CEES exposure attenuated CEES-induced DNA damage in these cells. Similar AEOL 10150 treatments also caused significant (p < 0.05) reversal of CEES-induced decreases in cell viability in normal human epidermal keratinocytes. Cytoplasmic and mitochondrial reactive oxygen species measurements showed that AEOL 10150 treatment drastically ameliorated the CEES-induced oxidative stress in both JB6 and HaCaT cells. Based on AEOL 10150 pharmacokinetic studies in SKH-1 mouse skin, mice were treated with a topical formulation plus subcutaneous injection (5mg/kg) of AEOL 10150 1h after CEES (4mg/mouse) exposure and every 4h thereafter for 12h. This AEOL 10150 treatment regimen resulted in over 50% (p < 0.05) reversal of CEES-induced skin bi-fold and epidermal thickness, myeloperoxidase activity, and DNA oxidation in mouse skin. Results from this study demonstrate the potential therapeutic efficacy of AEOL 10150 against CEES-mediated cutaneous lesions, supporting AEOL 10150 as a medical countermeasure against SM-induced skin injuries.
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