Biochemical Alterations in Rat Lung Lavage Fluid Following Acute Sulfur Mustard Inhalation: Ii. Increases in Proteolytic Activity

Clar, Fred M. Cowan Dana R. Anderson

doi:10.1080/089583797198411

Cited by 12 publications

(3 citation statements)

References 18 publications

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“…During the next 12 hours, the main objective clinical findings develop with increasing cough, tachypnea, sinus pain [20,21]. Bronchiolar obstruction vs. bronchospasm can be anticipated due to pseudomembrane formation within the airways, sloughing of epithelium, and lower airway obstruction.…”

Section: Methodsmentioning

confidence: 99%

“…In spirometric findings, more obstructive patterns than restriction have been shown (53% vs. 2%) [19]. Generally, abnormal pulmonary function tests and particularly restrictive patterns tend to worsen over time [21]. …”

Section: Methodsmentioning

confidence: 99%

“…There is some evidence for the role for proteases such as serine, cysteine, and MMP in the pathogenesis of SM-induced damage, even in the SM exposed model [21,44]. SM inhalation may cause cell death of airway macrophages by themselves, as well as degenerated chemotactic and phagocytic functions of the surviving cells.…”

Section: Methodsmentioning

confidence: 99%

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Treatment for sulfur mustard lung injuries; new therapeutic approaches from acute to chronic phase

et al. 2012

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ObjectiveSulfur mustard (SM) is one of the major potent chemical warfare and attractive weapons for terrorists. It has caused deaths to hundreds of thousands of victims in World War I and more recently during the Iran-Iraq war (1980–1988). It has ability to develop severe acute and chronic damage to the respiratory tract, eyes and skin. Understanding the acute and chronic biologic consequences of SM exposure may be quite essential for developing efficient prophylactic/therapeutic measures. One of the systems majorly affected by SM is the respiratory tract that numerous clinical studies have detailed processes of injury, diagnosis and treatments of lung. The low mortality rate has been contributed to high prevalence of victims and high lifetime morbidity burden. However, there are no curative modalities available in such patients. In this review, we collected and discussed the related articles on the preventive and therapeutic approaches to SM-induced respiratory injury and summarized what is currently known about the management and therapeutic strategies of acute and long-term consequences of SM lung injuries.MethodThis review was done by reviewing all papers found by searching following key words sulfur mustard; lung; chronic; acute; COPD; treatment.ResultsMustard lung has an ongoing pathological process and is active disorder even years after exposure to SM. Different drug classes have been studied, nevertheless there are no curative modalities for mustard lung.ConclusionComplementary studies on one hand regarding pharmacokinetic of drugs and molecular investigations are mandatory to obtain more effective treatments.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Treatment for sulfur mustard lung injuries; new therapeutic approaches from acute to chronic phase

et al. 2012

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Prophylactic protection by N‐acetylcysteine against the pulmonary injury induced by 2‐chloroethyl ethyl sulfide, a mustard analogue

Das

Mukherjee

Smith³

et al. 2003

J Biochem & Molecular Tox

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Mustard gas exposure causes adult respiratory distress syndrome associated with lung injury. The purpose of this study was to investigate whether an antioxidant, such as N-acetylcysteine (NAC), has any protective effect. Guinea pigs were given single exposure (0.5-6 mg/kg body weight) of 2-chloroethyl ethyl sulfide (CEES) as a mustard analogue intratracheally and maintained for various lengths of time (1 h to 21 days). Within 1 h of CEES infusion at 4 mg/kg, high levels of tumor necrosis factor alpha (TNF-alpha), ceramides, and nuclear factor kappaB accumulated in lung and alveolar macrophages. Both acid and neutral sphingomyelinases were activated within 4 h. These signal transduction events were associated with alteration in the oxygen defense system. Within 1 h of exposure to CEES (6 mg/kg body weight), there was 10-fold increase in the (125)I-BSA leakage into lung tissue, indicating severe lung injury. Although low level of CEES exposure (0.5 mg/kg body weight) produced symptoms of chemical burn in lung as early as 1 h after exposure, the severity of edema, congestion, hemorrhage, and inflammation increased progressively with time (1 h to 21 days). Feeding of single dose of NAC (0.5 g) by gavage just before the CEES infusion was ineffective to counteract these effects. However, consumption of the antioxidant in drinking water for 3 or 30 days prior to CEES exposure significantly inhibited the induction of TNF-alpha, activation of neutral and acid sphingomyelinases, production of ceramides, activation of caspases, leakage of (125)I-bovine serum albumin ((125)I-BSA) into lung tissue, and histological alterations in lung. Pretreatment with NAC for 3 and 30 days protected against 69-76% of the acute lung injury. Therefore, NAC may be an antidote for CEES-induced lung injury.

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Treatment of Pulmonary Complications in Chemical Patients

Ghanei

Harandi

2016

Mustard Lung

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Biochemical Alterations in Rat Lung Lavage Fluid Following Acute Sulfur Mustard Inhalation: Ii. Increases in Proteolytic Activity

Cited by 12 publications

References 18 publications

Treatment for sulfur mustard lung injuries; new therapeutic approaches from acute to chronic phase

Treatment for sulfur mustard lung injuries; new therapeutic approaches from acute to chronic phase

Prophylactic protection by N‐acetylcysteine against the pulmonary injury induced by 2‐chloroethyl ethyl sulfide, a mustard analogue

Treatment of Pulmonary Complications in Chemical Patients

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