Mechanism of acute lung injury due to phosgene exposition and its protection by cafeic acid phenethyl ester in the rat

Wang, Peng; Ye, Xiao-long; Liu, Rui; Chen, Hongli; Liang, Xin; Li, Wenli; Zhang, Xiaodi; Qin, Xu-Jun; Bai, Hua; Zhang, Wei; Wang, Xin; Hai, Chen

doi:10.1016/j.etp.2011.10.001

Cited by 27 publications

(25 citation statements)

References 40 publications

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“…the only antioxidant enzyme which scavenges superoxide, and GSH is one of the major components of the nonenzymatic antioxidant system. Both of them have been reported to be markedly decreased in sepsis-induced ALI(34,35). In our study, C3G caused a remarkable reduction in MDA level and a significantly increase in SOD activity and GSH content in lungs of CLP rats.…”

mentioning

confidence: 56%

Cyanidin-3-O-glucoside attenuates acute lung injury in sepsis rats

XueRui

et al. 2015

Journal of Surgical Research

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confidence: 56%

Cyanidin-3-O-glucoside attenuates acute lung injury in sepsis rats

XueRui

et al. 2015

Journal of Surgical Research

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“…Several studies have evaluated the therapeutic value of antioxidant compounds against phosgene toxicity [20, 21, 99–102], and while it seems that pre-exposure administration of antioxidants may provide substantial protection against phosgene toxicity, protection is rarely afforded if administered PE. The lack of PE efficacy may be attributed to the inability of these antioxidant compounds to reach a body-burden level that is sufficient to detoxify phosgene-induced oxidative radicals at a sufficiently high rate and within a short duration so as to prevent oxidant-induced pulmonary injury.…”

Section: 0 Results and Discussionmentioning

confidence: 99%

“…Two antioxidant compounds, n-acetylcysteine (NAC) and caffeic acid phenethyl ester (CAPE), have been shown to reduce phosgene toxicity when administered PE. Both NAC and CAPE were able to reduce lung edema and improve biochemical markers of lung injury, such as glutathione, superoxide dismutase, and lipid peroxidation, following phosgene inhalation [20, 101, 102]. The mechanism by which these compounds provide protection against phosgene toxicity may be due to their ability to act directly as an antioxidant as well as their ability to activate the Nrf2 pathway.…”

Section: 0 Results and Discussionmentioning

confidence: 99%

Conceptual approaches for treatment of phosgene inhalation-induced lung injury

Holmes¹,

Keyser²,

Paradiso³

et al. 2016

Toxicology Letters

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Toxic industrial chemicals are used throughout the world to produce everyday products such as household and commercial cleaners, disinfectants, pesticides, pharmaceuticals, plastics, paper, and fertilizers. These chemicals are produced, stored, and transported in large quantities, which poses a threat to the local civilian population in cases of accidental or intentional release. Several of these chemicals have no known medical countermeasures for their toxic effects. Phosgene is a highly toxic industrial chemical which was used as a chemical warfare agent in WWI. Exposure to phosgene causes latent, non-cardiogenic pulmonary edema which can result in respiratory failure and death. The mechanisms of phosgene-induced pulmonary injury are not fully identified, and currently there is no efficacious countermeasure. Here, we provide a proposed mechanism of phosgene-induced lung injury based on the literature and from studies conducted in our lab, as well as provide results from studies designed to evaluate survival efficacy of potential therapies following whole-body phosgene exposure in mice. Several therapies were able to significantly increase 24 hr survival following an LCt50–70 exposure to phosgene; however, no treatment was able to fully protect against phosgene-induced mortality. These studies provide evidence that mortality following phosgene toxicity can be mitigated by neuro- and calcium-regulators, antioxidants, phosphodiesterase and endothelin receptor antagonists, angiotensin converting enzymes, and transient receptor potential cation channel inhibitors. However, because the mechanism of phosgene toxicity is multifaceted, we conclude that a single therapeutic is unlikely to be sufficient to ameliorate the multitude of direct and secondary toxic effects caused by phosgene inhalation.

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“…The exact means of phosgene induced injury remains unclear though studies indicate that oxidative stress is likely a primary mechanism of toxicity[36]. Increases in markers of lipid oxidation and decreases in GSH are observable in rat lung tissue after inhalation exposures to phosgene gas[37] .…”

Section: 0 Overview Of the Evidence For Oxidative Stress In Cwas Anmentioning

confidence: 99%

Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals

McElroy

Day

2016

Biochemical Pharmacology

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The continuing horrors of military conflicts and terrorism often involve the use of chemical warfare agents (CWAs) and toxic industrial chemicals (TICs). Many CWA and TIC exposures are difficult to treat due to the danger they pose to first responders and their rapid onset that can produce death shortly after exposure. While the specific mechanism(s) of toxicity of these agents are diverse, many are associated either directly or indirectly with increased oxidative stress in affected tissues. This has led to the exploration of various antioxidants as potential medical countermeasures for CWA/TIC exposures. Studies have been performed across a wide array of agents, model organisms, exposure systems, and antioxidants, looking at an almost equally diverse set of endpoints. Attempts at treating CWAs/TICs with antioxidants have met with mixed results, ranging from no effect to nearly complete protection. The aim of this commentary is to summarize the literature in each category for evidence of oxidative stress and antioxidant efficacy against CWAs and TICs. While there is great disparity in the data concerning methods, models, and remedies, the outlook on antioxidants as medical countermeasures for CWA/TIC management appears promising.

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Mechanism of acute lung injury due to phosgene exposition and its protection by cafeic acid phenethyl ester in the rat

Cited by 27 publications

References 40 publications

Cyanidin-3-O-glucoside attenuates acute lung injury in sepsis rats

Cyanidin-3-O-glucoside attenuates acute lung injury in sepsis rats

Conceptual approaches for treatment of phosgene inhalation-induced lung injury

Antioxidants as potential medical countermeasures for chemical warfare agents and toxic industrial chemicals

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