Posttreatment with Eicosatetraynoic Acid Decreases Lung Edema in Guinea Pigs Exposed to Phosgene: The Role of Leukotrienes

Sciuto, Alfred M.; Stotts, Richard R.

doi:10.3109/01902149809041535

Cited by 8 publications

(9 citation statements)

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“…It was reported recently that ETYA caused a reduction in edema formation in the isolated perfused guinea pig lung within 3 h of exposure to phosgene (Sciuto & Stotts, 1998). However the reason(s) for this effect could not be explained by the usual mechanistic action of ETYA, that is, as a lipoxygenase inhibitor (Farrukh et al, 1988;Kühn et al, 1984).…”

Section: Discussionmentioning

confidence: 78%

“…data published earlier (Sciuto & Stotts, 1998, Figure 5). Only lung tissue from experiments that had both the GSH and TBARS measurements were used to calculate the ratio.…”

Section: Inhalation Toxicology Downloaded From Informahealthcarecom mentioning

confidence: 72%

“…Lung Tissue Wet/Dry Weight Determination In addition to measuring edema by real-time lung weight gain changes (Sciuto & Stotts, 1998), pulmonary edema formation (PEF) can be estimated gravimetrically by determining the lung wet weight to lung dry weight ratio. Wet/dry (W/D) weight ratios were measured on lungs at the conclusion of the 100-min perfusion period (180 min postexposure time).…”

Section: Methodsmentioning

confidence: 99%

“…This assay combined the techniques from several sources (Buege & Aust, 1978;Uchiyama & Mihara, 1978;Wong et al, 1982). The procedure has been described previously (Sciuto & Stotts, 1998). To check the accuracy of the assay, standards using 1,1,3,3-tetraethylpropane (TEP) were processed in a similar manner.…”

Section: Methodsmentioning

confidence: 99%

“…The primary effect of treatment with ETYA in these models is related to its inhibition of permeability-enhancing leukotrienes thought to be important in oxidant lung injury in the rabbit (Farrukh et al, 1988;Guo et al, 1990). In a more recent study, while ETYA prevented increases in PEF, it was not effective in ameliorating perfusate leukotriene formation in the isolated perfused guinea pig lung (Sciuto & Stotts, 1998). The efficacy of ETYA treatment may be associated with a common mechanism of protection not described using in vivo animal models.…”

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confidence: 87%

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Posttreatment With Etya Protects Against Phosgene-Induced Lung Injury by Amplifying the Glutathione to Lipid Peroxidation Ratio

Sciuto

2000

Inhalation Toxicology

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Exposure to phosgene has been shown to cause severe and life-threatening pulmonary edema. There is evidence that successful treatment of phosgene-induced acute lung injury may be related to increased antioxidant activity. Acetylenic acids such as 5,8,11, 14-eicosatetraynoic acid (ETYA) have been shown to be effective in preventing pulmonary edema formation (PEF). In phosgene-exposed guinea pigs, we examined the effects of ETYA on PEF. Lipid peroxidation (thiobarbituric acid-reactive substance, TBARS) and total glutathione (GSH) were measured in lung tissue from isolated, buffer-perfused guinea pig lungs at 180 min after start of exposure. Guinea pigs were challenged with 175 mg/m(3) (44 ppm) phosgene for 10 min (1750 mg( small middle dot)min/m(3)). Five minutes after removal from the exposure chamber, guinea pigs were treated, ip, with 200 microl of 100 microM ETYA in ethanol (ETOH). Two hundred microliters of 50 microM ETYA in ETOH was added to the 200 ml perfusate every 40 min beginning at 60 min after start of exposure (t = 0). There were four groups in this study: air-exposed, phosgene-exposed, phosgene + ETYA-posttreated, and air + ETYA-posttreated. Posttreatment with ETYA prevented GSH depletion, 2. 7 +/- 0.5 micromol/mg protein versus 1 +/- 0.2 micromol/mg protein, for the untreated phosgene-exposed lungs (p < or =.05). ETYA posttreatment also significantly decreased PEF (p

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Section: Discussionmentioning

confidence: 78%

“…data published earlier (Sciuto & Stotts, 1998, Figure 5). Only lung tissue from experiments that had both the GSH and TBARS measurements were used to calculate the ratio.…”

Section: Inhalation Toxicology Downloaded From Informahealthcarecom mentioning

confidence: 72%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 87%

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Posttreatment With Etya Protects Against Phosgene-Induced Lung Injury by Amplifying the Glutathione to Lipid Peroxidation Ratio

Sciuto

2000

Inhalation Toxicology

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Toxicology of Chemical Warfare Agents

Maynard¹,

Chilcott²

2009

General, Applied and Systems Toxicology

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Irritant or toxic chemicals have been used in warfare since ancient times and a number of international laws have attempted to prevent the use of such weapons. However, chemical warfare agents remain to be a global threat and so it is important to maintain an understanding of their mechanism of action, their clinical effects and to identify effective treatment regimes. Chemical warfare agents have traditionally been classified according to their medical effect(s) or military application. Vesicant agents (for example, sulphur mustard and lewisite) are highly potent acute contact irritants and may cause severe skin damage following dermal exposure as well as extensive damage to other epithelial surfaces (such as the lungs and eyes). Vesicants are generally considered to be non‐lethal in that they cause debilitating (rather than fatal) injuries. Indeed, some chemicals are used specifically for their irritating (rather than lethal) effects. For example, the riot control agents CS and CR are potent lachrymators but generally lack any significant, systemic toxicity following respiratory or dermal exposure. In contrast, a number of chemicals have been specifically developed or used on account of their lethality and these include the nerve agents (such as sarin, tabun, soman and VX), lung damaging agents (phosgene and chlorine) and other systemic poisons such as cyanides. A large miscellany of other, more exotic chemicals exist and these include endogenous bioregulators as well as plant, animal, marine and fungal toxins.

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Effect of dietary treatment with n‐propyl gallate or vitamin E on the survival of mice exposed to phosgene

Sciuto¹,

Moran²

2001

J of Applied Toxicology

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Phosgene, widely used in industrial processes, can cause life-threatening pulmonary edema and acute lung injury. One mechanism of protection against phosgene-induced lung injury may involve the use of antioxidants. The present study focused on dietary supplementation in mice using n-propyl gallate (nPG)--a gallate acid ester compound used in food preservation--and vitamin E. Five groups of male mice were studied: group 1, control-fed with Purina rodent chow 5002; group 2, fed 0.75% nPG (w/w) in 5002; group 3, fed 1.5% nPG (w/w) in 5002; group 4 fed 1% (w/w) vitamin E in 5002; and group 5, fed 2% (w/w) vitamin E also in 5002. Mice were fed for 23 days. On day 23 mice were exposed to 32 mg m-3 (8 ppm) phosgene for 20 min (640 mg. min m-3) in a whole-body exposure chamber. Survival rates were determined at 12 and 24 h. In mice that died within 12 h, the lungs were removed and lung wet weights, dry weights, wet/dry weight ratios, lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and glutathione (GSH) were assessed. Vitamin E had no positive effect on any outcome measured. There was no significant difference between 1.5% nPG and any parameter measured or survival rate compared with 5002 + phosgene. However, dietary treatment with 0.75% nPG significantly increased survival rate (P

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Posttreatment with Eicosatetraynoic Acid Decreases Lung Edema in Guinea Pigs Exposed to Phosgene: The Role of Leukotrienes

Cited by 8 publications

References 48 publications

Posttreatment With Etya Protects Against Phosgene-Induced Lung Injury by Amplifying the Glutathione to Lipid Peroxidation Ratio

Posttreatment With Etya Protects Against Phosgene-Induced Lung Injury by Amplifying the Glutathione to Lipid Peroxidation Ratio

Toxicology of Chemical Warfare Agents

Effect of dietary treatment with n‐propyl gallate or vitamin E on the survival of mice exposed to phosgene

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