ArticleFree radical biology & medicine2010
Treatment with the catalytic metalloporphyrin AEOL 10150 reduces inflammation and oxidative stress due to inhalation of the sulfur mustard analog 2-chloroethyl ethyl sulfide.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 70 citations in OpenAlex.
- Oxidative Stress: An Intersection Between Radiation and Sulfur Mustard Lung Injury.Disaster medicine and public health preparedness · 2024Article
- Novel Catalytic Antioxidant Formulation Decreases Oxidative Stress, Neuroinflammation and Cognitive Dysfunction in a Model of Nerve Agent Intoxication.The Journal of pharmacology and experimental therapeutics · 2024Article
- Epigenetic mechanisms of alveolar macrophage activation in chemical-induced acute lung injury.Frontiers in immunology · 2024Review
- Overlapping Science in Radiation and Sulfur Mustard Exposures of Skin and Lung: Consideration of Models, Mechanisms, Organ Systems, and Medical Countermeasures: Overlapping science in radiation and sulfur mustard injuries to lung and skin.Disaster medicine and public health preparedness · 2023Article
- A review of chemical warfare agents linked to respiratory and neurological effects experienced in Gulf War Illness.Inhalation toxicology · 2022Review
- Antioxidant drug therapy as a neuroprotective countermeasure of nerve agent toxicity.Neurobiology of disease · 2020Review
- Neuroprotective effects of a catalytic antioxidant in a rat nerve agent model.Redox biology · 2019Article
- Improvements in SOD mimic AEOL-10150, a potent broad-spectrum antioxidant.Military Medical Research · 2018Review
- TRPA1 and CGRP antagonists counteract vesicant-induced skin injury and inflammation.Toxicology letters · 2018Article
- Neuroprotective Effects of AEOL10150 in a Rat Organophosphate Model.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Scavenging reactive oxygen species inhibits status epilepticus-induced neuroinflammation.Experimental neurology · 2017Article
- An Official American Thoracic Society Workshop Report: Chemical Inhalational Disasters. Biology of Lung Injury, Development of Novel Therapeutics, and Medical Preparedness.Annals of the American Thoracic Society · 2017Article
- From the Cover: Catalytic Antioxidant Rescue of Inhaled Sulfur Mustard Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Plasma cysteine/cystine redox couple disruption in animal models of temporal lobe epilepsy.Redox biology · 2016Article
- Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 2016Review
- Sulfur mustard inhalation: mechanisms of injury, alteration of coagulation, and fibrinolytic therapy.Annals of the New York Academy of Sciences · 2016Review
- Macrophages and inflammatory mediators in pulmonary injury induced by mustard vesicants.Annals of the New York Academy of Sciences · 2016Review
- Emerging targets for treating sulfur mustard-induced injuries.Annals of the New York Academy of Sciences · 2016Review
- Inflammatory mechanisms of pulmonary injury induced by mustards.Toxicology letters · 2016Review
- Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals.Biochemical pharmacology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Sulfur mustard (bis-2-(chloroethyl) sulfide; SM) is a highly reactive vesicating and alkylating chemical warfare agent. A SM analog, 2-chloroethyl ethyl sulfide (CEES), has been utilized to elucidate mechanisms of toxicity and as a screen for therapeutics. Previous studies with SM and CEES have demonstrated a role for oxidative stress as well as decreased injury with antioxidant treatment. We tested whether posttreatment with the metalloporphyrin catalytic antioxidant AEOL 10150 would improve outcome in CEES-induced lung injury. Anesthetized rats inhaled 5% CEES for 15 min via a nose-only inhalation system. At 1 and 9 h after CEES exposure, rats were given AEOL 10150 (5 mg/kg, sc). At 18 h post-CEES exposure BALF lactate dehydrogenase activity, protein, IgM, red blood cells, and neutrophils were elevated but were decreased by AEOL 10150 treatment. Lung myeloperoxidase activity was increased after CEES inhalation and was ameliorated by AEOL 10150. The lung oxidative stress markers 8-OHdG and 4-HNE were elevated after CEES exposure and significantly decreased by AEOL 10150 treatment. These findings demonstrate that CEES inhalation increased lung injury, inflammation, and oxidative stress, and AEOL 10150 was an effective rescue agent. Further investigation utilizing catalytic antioxidants as treatment for SM inhalation injury is warranted.
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