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Article ; Online: Pulmonary toxicity following inhalation exposure to VX in anesthetized rats: Possible roles for compromised immunity and oxidative stress-induced lung injury.

Sciuto, Alfred M / Peng, Xinqi

2019 Volume 44, Issue 8-9, Page(s) 379–396

Abstract: ... increased at 6 h post-inhalation for the 31.6 mg/m ... 1 µm. Following exposure, all rats were removed from the ventilator and allowed to recover ...

Abstract	The nerve agent VX is one of the most deadly threat agents available in weapons stockpiles for intentional release. While mostly considered a percutaneous toxicant, it can be fatal when aerosolized. The objective of this study was to investigate toxic responses in the lung up to two weeks following a single 10-minute exposure to inhaled VX. Anesthetized rats were exposed singly and only once to VX. The nebulization rate in this system was 0.2-0.3 ml per minute with the delivery of a consistent particle size of 2.1 µm. Following exposure, all rats were removed from the ventilator and allowed to recover in the glovebox for 10-15 minutes. Results showed that inhaled VX altered several respiratory parameters and caused increased lung resistance up to 6 h post-exposure (PE). There was a trending increase in SOD and xanthine oxidoreductase (XOR) activities, both of which are indicative of oxidative stress. Based on increased lung tissue p38 signaling, MAP kinase expression was activated after VX exposure. IL-6 expression was also increased at 6 h post-inhalation for the 31.6 mg/m
MeSH term(s)	Acetylcholinesterase/metabolism ; Administration, Inhalation ; Animals ; Bronchoalveolar Lavage Fluid ; Chemical Warfare Agents/toxicity ; Cholinesterase Inhibitors/toxicity ; Inhalation Exposure/adverse effects ; Lung Injury/chemically induced ; Nitric Oxide Synthase Type II/metabolism ; Organothiophosphorus Compounds/toxicity ; Oxidative Stress ; Pulmonary Surfactants ; Rats ; Superoxide Dismutase/metabolism ; Xanthine Dehydrogenase/metabolism
Chemical Substances	Chemical Warfare Agents ; Cholinesterase Inhibitors ; Organothiophosphorus Compounds ; Pulmonary Surfactants ; VX (9A4381183B) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Superoxide Dismutase (EC 1.15.1.1) ; Xanthine Dehydrogenase (EC 1.17.1.4) ; Acetylcholinesterase (EC 3.1.1.7)
Language	English
Publishing date	2019-02-22
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	603791-4
ISSN	1521-0499 ; 0190-2148
ISSN (online)	1521-0499
ISSN	0190-2148
DOI	10.1080/01902148.2018.1519003
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Article ; Online: Evaluation of an in vitro screening model to assess phosgene inhalation injury.

Olivera, Dorian S / Hoard-Fruchey, Heidi / Sciuto, Alfred M

Toxicology mechanisms and methods

2017 Volume 27, Issue 1, Page(s) 45–51

Abstract: Therapeutic development against exposure to toxic gases is hindered by the lack of appropriate models to evaluate candidate compounds prior to animal efficacy studies. In this study, an in vitro, air-liquid interface exposure model has been tested to ... ...

Abstract	Therapeutic development against exposure to toxic gases is hindered by the lack of appropriate models to evaluate candidate compounds prior to animal efficacy studies. In this study, an in vitro, air-liquid interface exposure model has been tested to examine its potential application for screening treatments for phosgene (carbonyl chloride)-induced pulmonary injury. Epithelial cultures on Transwell
MeSH term(s)	Acute Lung Injury/chemically induced ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Bronchi/cytology ; Bronchi/drug effects ; Bronchi/metabolism ; Cell Culture Techniques ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Electric Impedance ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Glucose/metabolism ; Glutamine/metabolism ; Humans ; Inhalation Exposure/adverse effects ; Models, Biological ; Phosgene/toxicity
Chemical Substances	Glutamine (0RH81L854J) ; Phosgene (117K140075) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2081252-8
ISSN	1537-6524 ; 1537-6516 ; 1051-7235
ISSN (online)	1537-6524
ISSN	1537-6516 ; 1051-7235
DOI	10.1080/15376516.2016.1243183
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Zs.A 3215: Show issues

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Article ; Online: Transcriptomic Characterization of Inhalation Phosphine Toxicity in Adult Male Sprague-Dawley Rats.

Hartog, Matthew A / Lewandowski, Rebecca J / Hofmann, Christopher S / Melber, Ashley A / Rothwell, Cristin C / Sherman, Katherine / Andres, Jaclynn / Tressler, Justin A / Sciuto, Alfred M / Wong, Benjamin / Hoard-Fruchey, Heidi M

Chemical research in toxicology

2021 Volume 34, Issue 9, Page(s) 2032–2044

Abstract: Phosphine ( ... ...

Abstract	Phosphine (PH
MeSH term(s)	Administration, Inhalation ; Animals ; Antihypertensive Agents/pharmacology ; Apelin/metabolism ; Cardiomegaly/chemically induced ; Cardiotonic Agents/pharmacology ; Cardiotoxicity/genetics ; Cardiotoxicity/metabolism ; Heart/drug effects ; Male ; Pesticides/toxicity ; Phosphines/administration & dosage ; Phosphines/toxicity ; Rats, Sprague-Dawley ; Rodenticides/administration & dosage ; Rodenticides/toxicity ; Signal Transduction/drug effects ; Transcriptome/drug effects ; Rats
Chemical Substances	Antihypertensive Agents ; Apelin ; Apln protein, rat ; Cardiotonic Agents ; Pesticides ; Phosphines ; Rodenticides ; phosphine (FW6947296I)
Language	English
Publishing date	2021-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.1c00108
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Article ; Online: Effects of inhaled aerosolized carfentanil on real-time physiological responses in mice: a preliminary evaluation of naloxone.

Wong, Benjamin / Perkins, Michael W / Tressler, Justin / Rodriguez, Ashley / Devorak, Jennifer / Sciuto, Alfred M

Inhalation toxicology

2017 Volume 29, Issue 2, Page(s) 65–74

Abstract: ... CD-1 mice (25-30 g) were exposed to 0.4 or 4.0 mg/m ...

Abstract	This study examined the real-time exposure-response effects of aerosolized carfentanil (CRF) on opioid-induced toxicity, respiratory dynamics and cardiac function in mice. Unrestrained, conscious male CD-1 mice (25-30 g) were exposed to 0.4 or 4.0 mg/m
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Journal Article
ZDB-ID	1038809-6
ISSN	1091-7691 ; 0895-8378
ISSN (online)	1091-7691
ISSN	0895-8378
DOI	10.1080/08958378.2017.1282065
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Article ; Online: Changes in murine respiratory dynamics induced by aerosolized carfentanil inhalation: Efficacy of naloxone and naltrexone.

Tuet, Wing Y / Pierce, Samuel A / Racine, Michelle C / Tressler, Justin / McCranor, Bryan J / Sciuto, Alfred M / Wong, Benjamin

Toxicology letters

2019 Volume 316, Page(s) 127–135

Abstract: ... investigated using adult male CD-1 mice. Mice were exposed to 0.4 mg/m ...

Abstract	Carfentanil (CRF) is an extremely potent opioid capable of inducing fatal respiratory depression. Naloxone (NX) and naltrexone (NTX) are opioid antagonists for which the efficacy against CRF remains largely unexplored. In this study, the effects of aerosolized CRF on respiratory function were investigated using adult male CD-1 mice. Mice were exposed to 0.4 mg/m
MeSH term(s)	Administration, Inhalation ; Aerosols ; Analgesics, Opioid/administration & dosage ; Analgesics, Opioid/pharmacokinetics ; Analgesics, Opioid/toxicity ; Animals ; Computer Simulation ; Dose-Response Relationship, Drug ; Fentanyl/administration & dosage ; Fentanyl/analogs & derivatives ; Fentanyl/pharmacokinetics ; Fentanyl/toxicity ; Humans ; Lung/drug effects ; Lung/physiopathology ; Male ; Mice ; Models, Biological ; Naloxone/administration & dosage ; Naltrexone/administration & dosage ; Narcotic Antagonists/administration & dosage ; Plethysmography, Whole Body ; Respiration/drug effects ; Respiratory Insufficiency/chemically induced ; Respiratory Insufficiency/physiopathology ; Respiratory Insufficiency/prevention & control ; Risk Assessment
Chemical Substances	Aerosols ; Analgesics, Opioid ; Narcotic Antagonists ; Naloxone (36B82AMQ7N) ; Naltrexone (5S6W795CQM) ; carfentanil (LA9DTA2L8F) ; Fentanyl (UF599785JZ)
Language	English
Publishing date	2019-09-17
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2019.09.012
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Zs.A 1367: Show issues

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Article ; Online: Phosphine toxicity: a story of disrupted mitochondrial metabolism.

Sciuto, Alfred M / Wong, Benjamin J / Martens, Margaret E / Hoard-Fruchey, Heidi / Perkins, Michael W

Annals of the New York Academy of Sciences

2016 Volume 1374, Issue 1, Page(s) 41–51

Abstract: Rodenticides and pesticides pose a significant threat not only to the environment but also directly to humans by way of accidental and/or intentional exposure. Metal phosphides, such as aluminum, magnesium, and zinc phosphides, have gained popularity ... ...

Abstract	Rodenticides and pesticides pose a significant threat not only to the environment but also directly to humans by way of accidental and/or intentional exposure. Metal phosphides, such as aluminum, magnesium, and zinc phosphides, have gained popularity owing to ease of manufacture and application. These agents and their hydrolysis by-product phosphine gas (PH3 ) are more than adequate for eliminating pests, primarily in the grain storage industry. In addition to the potential for accidental exposures in the manufacture and use of these agents, intentional exposures must also be considered. As examples, ingestion of metal phosphides is a well-known suicide route, especially in Asia; and intentional release of PH3 in a populated area cannot be discounted. Metal phosphides cause a wide array of effects that include cellular poisoning, oxidative stress, cholinesterase inhibition, circulatory failure, cardiotoxicity, gastrointestinal and pulmonary toxicity, hepatic damage, neurological toxicity, electrolyte imbalance, and overall metabolic disturbances. Mortality rates often exceed 70%. There are no specific antidotes against metal phosphide poisoning. Current therapeutic intervention is limited to supportive care. The development of beneficial medical countermeasures will rely on investigative mechanistic toxicology; the ultimate goal will be to identify specific treatments and therapeutic windows for intervention.
MeSH term(s)	Animals ; Cell Death/drug effects ; Humans ; Mitochondria/drug effects ; Mitochondria/metabolism ; Models, Biological ; Oxidative Stress/drug effects ; Phosphines/toxicity ; Reactive Oxygen Species/metabolism
Chemical Substances	Phosphines ; Reactive Oxygen Species ; phosphine (FW6947296I)
Language	English
Publishing date	2016-05-24
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.13081
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Article ; Online: Measurement of various respiratory dynamics parameters following acute inhalational exposure to soman vapor in conscious rats.

Perkins, Michael W / Wong, Benjamin / Rodriguez, Ashley / Devorak, Jennifer / Sciuto, Alfred M

Inhalation toxicology

2015 Volume 27, Issue 9, Page(s) 432–439

Abstract: ... 560 and 600 mg × min/m(3) of soman vapor in a customized inhalational exposure system. Various ... animals, with significant increases in both at 24 h following exposure to 600 mg × min/m(3). Exposure ... to soman resulted in increases in respiratory frequency (RF) in animals exposed to 560 and 600 mg × min/m(3 ...

Abstract	Respiratory dynamics were investigated in head-out plethysmography chambers following inhalational exposure to soman in untreated, non-anesthetized rats. A multipass saturator cell was used to generate 520, 560 and 600 mg × min/m(3) of soman vapor in a customized inhalational exposure system. Various respiratory dynamic parameters were collected from male Sprague-Dawley rats (300--350 g) during (20 min) and 24 h (10 min) after inhalational exposure. Signs of CWNA-induced cholinergic crisis were observed in all soman-exposed animals. Percentage body weight loss and lung edema were observed in all soman-exposed animals, with significant increases in both at 24 h following exposure to 600 mg × min/m(3). Exposure to soman resulted in increases in respiratory frequency (RF) in animals exposed to 560 and 600 mg × min/m(3) with significant increases following exposure to 560 mg × min/m(3) at 24 h. No significant alterations in inspiratory time (IT) or expiratory time (ET) were observed in soman-exposed animals 24 h post-exposure. Prominent increases in tidal volume (TV) and minute volume (MV) were observed at 24 h post-exposure in animals exposed to 600 mg × min/m(3). Peak inspiratory (PIF) and expiratory flow (PEF) followed similar patterns and increased 24 h post-exposure to 600 mg × min/m(3) of soman. Results demonstrate that inhalational exposure to 600 mg × min/m(3) soman produces notable alterations in various respiratory dynamic parameters at 24 h. The following multitude of physiological changes in respiratory dynamics highlights the need to develop countermeasures that protect against respiratory toxicity and lung injury.
MeSH term(s)	Administration, Inhalation ; Animals ; Biomarkers ; Cholinesterase Inhibitors/toxicity ; Fluorocarbons/administration & dosage ; Fluorocarbons/adverse effects ; Gas Poisoning/physiopathology ; Male ; Nerve Agents/toxicity ; Organophosphate Poisoning/physiopathology ; Pharmaceutical Vehicles/administration & dosage ; Pharmaceutical Vehicles/adverse effects ; Pulmonary Edema/etiology ; Pulmonary Ventilation/drug effects ; Rats, Sprague-Dawley ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/physiopathology ; Respiratory Mucosa/secretion ; Respiratory Rate/drug effects ; Respiratory System/drug effects ; Respiratory System/physiopathology ; Rhinitis/etiology ; Seizures/etiology ; Soman/toxicity ; Tidal Volume/drug effects ; Volatilization ; Weight Loss/drug effects
Chemical Substances	Biomarkers ; Cholinesterase Inhibitors ; Fluorocarbons ; Nerve Agents ; Pharmaceutical Vehicles ; Soman (96-64-0) ; perflexane (FX3WJ41CMX)
Language	English
Publishing date	2015
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1038809-6
ISSN	1091-7691 ; 0895-8378
ISSN (online)	1091-7691
ISSN	0895-8378
DOI	10.3109/08958378.2015.1068890
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Article: The Cardiopulmonary Effects of Sodium Fluoroacetate (1080) in Sprague-Dawley Rats.

McCranor, Bryan J / Young, Talearia D / Tressler, Justin / Jennings, Laura / Irwin, James / Alli, Nazira A / Abilez, Marilynda K / Stone, Samuel / Racine, Michelle / Devorak, Jennifer L / Sciuto, Alfred M / Wong, Benjamin

Cogent biology

2019 Volume 5, Issue 1

Abstract: Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although ... ...

Abstract	Sodium fluoroacetate (1080) is a highly toxic metabolic poison that has the potential because of its lack of defined color, odor, and taste and its high water solubility to be intentionally or unintentionally ingested through food adulteration. Although the mechanism of action for 1080 has been known since the 1950's, no known antidote exists. In an effort to better understand the cardiopulmonary impacts of 1080, we utilized whole-body plethysmography and telemeterized Sprague-Dawley rats which allowed for the real-time measurement of respiratory and cardiac parameters following exposure using a non-invasive assisted-drinking method. Overall, the animals showed marked depression of respiratory parameters over the course of 24 hours post-exposure and the development of hemorrhage in the lung tissue. Tidal volume was reduced by 30% in males and 60% in females at 24 hours post-exposure, and respiratory frequency was significantly depressed as well. In telemeterized female rats, we observed severe cardiac abnormalities, highlighted by a 50% reduction in heart rate, 75% reduction in systolic blood pressure, and a 3.5-fold lengthening of the QRS interval over the course of 24 hours. We also observed a reduction in core body temperature of nearly 15°C. Our study was able to describe the severe and pronounced effects of sodium fluoroacetate poisoning on cardiopulmonary function, the results of which indicate that both tissue specific and systemic deficits contribute to the toxicological progression of 1080 intoxication and will need to be accounted for when developing any potential countermeasure for 1080 poisoning.
Language	English
Publishing date	2019-01-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2837326-1
ISSN	2331-2025
ISSN	2331-2025
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Article ; Online: Adverse respiratory effects in rats following inhalation exposure to ammonia: respiratory dynamics and histopathology.

Perkins, Michael W / Wong, Benjamin / Tressler, Justin / Rodriguez, Ashley / Sherman, Katherine / Andres, Jaclynn / Devorak, Jennifer / L Wilkins, William / Sciuto, Alfred M

Inhalation toxicology

2017 Volume 29, Issue 1, Page(s) 32–41

Abstract: Acute respiratory dynamics and histopathology of the lungs and trachea following inhaled exposure to ammonia were investigated. Respiratory dynamic parameters were collected from male Sprague-Dawley rats (300-350 g) during (20 min) and 24 h (10 min) ... ...

Abstract	Acute respiratory dynamics and histopathology of the lungs and trachea following inhaled exposure to ammonia were investigated. Respiratory dynamic parameters were collected from male Sprague-Dawley rats (300-350 g) during (20 min) and 24 h (10 min) after inhalation exposure for 20 min to 9000, 20,000, and 23,000 ppm of ammonia in a head-only exposure system. Body weight loss, analysis of blood cells, and lungs and trachea histopathology were assessed 1, 3, and 24 h following inhalation exposure to 20,000 ppm of ammonia. Prominent decreases in minute volume (MV) and tidal volume (TV) were observed during and 24 h post-exposure in all ammonia-exposed animals. Inspiratory time (IT) and expiratory time (ET) followed similar patterns and decreased significantly during the exposure and then increased at 24 h post-exposure in all ammonia-exposed animals in comparison to air-exposed controls. Peak inspiratory (PIF) and expiratory flow (PEF) significantly decreased during the exposure to all ammonia doses, while at 24 h post-exposure they remained significantly decreased following exposure to 20,000 and 23,000 ppm. Exposure to 20,000 ppm of ammonia resulted in body weight loss at 1 and 3 h post-exposure; weight loss was significant at 24 h compared to controls. Exposure to 20,000 ppm of ammonia for 20 min resulted in increases in the total blood cell counts of white blood cells, neutrophils, and platelets at 1, 3, and 24 h post-exposure. Histopathologic evaluation of the lungs and trachea tissue of animals exposed to 20,000 ppm of ammonia at 1, 3, and 24 h post-exposure revealed various morphological changes, including alveolar, bronchial, and tracheal edema, epithelial necrosis, and exudate consisting of fibrin, hemorrhage, and inflammatory cells. The various alterations in respiratory dynamics and damage to the respiratory system observed in this study further emphasize ammonia-induced respiratory toxicity and the relevance of efficacious medical countermeasure strategies.
Language	English
Publishing date	2017-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1038809-6
ISSN	1091-7691 ; 0895-8378
ISSN (online)	1091-7691
ISSN	0895-8378
DOI	10.1080/08958378.2016.1277571
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Article ; Online: Acute Gene Expression Profile of Lung Tissue Following Sulfur Mustard Inhalation Exposure in Large Anesthetized Swine.

Jugg, Bronwen J A / Hoard-Fruchey, Heidi / Rothwell, Cristin / Dillman, James F / David, Jonathan / Jenner, John / Sciuto, Alfred M

Chemical research in toxicology

2016 Volume 29, Issue 10, Page(s) 1602–1610

Abstract: Sulfur mustard (HD) is a vesicating and alkylating agent widely used on the battlefield during World War I and more recently in the Iran-Iraq War. It targets the eyes, skin, and lungs, producing skin burns, conjunctivitis, and compromised respiratory ... ...

Abstract	Sulfur mustard (HD) is a vesicating and alkylating agent widely used on the battlefield during World War I and more recently in the Iran-Iraq War. It targets the eyes, skin, and lungs, producing skin burns, conjunctivitis, and compromised respiratory function; early acute effects lead to long-term consequences. However, it is the effects on the lungs that drive morbidity and eventual mortality. The temporal postexposure response to HD within lung tissue raises the question of whether toxicity is driven by the alkylating properties of HD on critical homeostatic pathways. We have established an anesthetized swine model of inhaled HD vapor exposure to investigate the toxic effects of HD 12 h postexposure. Large white female swine were anesthetized and instrumented prior to exposure to air, 60 (sublethal) or 100 μg·kg
MeSH term(s)	Acetylcysteine/therapeutic use ; Administration, Inhalation ; Anesthesia ; Animals ; Dose-Response Relationship, Drug ; Female ; Gene Expression Profiling ; Inhalation Exposure ; Lung/drug effects ; Lung/metabolism ; Models, Animal ; Mustard Gas/administration & dosage ; Mustard Gas/toxicity ; Swine ; Toxicity Tests
Chemical Substances	Mustard Gas (T8KEC9FH9P) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2016-10-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.6b00069
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