Serum soluble Fas ligand and nitric oxide in long-term pulmonary complications induced by sulfur mustard: Sardasht-Iran Cohort Study

Ghazanfari, Tooba; Sharifnia, Zarin; Yaraee, Roya; Pourfarzam, Shahryar; Kariminia, Amina; Mahlojirad, Maryam; Faghihzadeh, Soghrat; Jalali-Nodoushan, Mohammad Reza; Ardestani, Sussan K.; Soroush, Mohammad Reza; Amiri, Sara; Hassan, Zuhair Mohammad; Ghavami, Saeid; Ghanei, Mostafa

doi:10.1016/j.intimp.2009.08.019

Cited by 20 publications

(8 citation statements)

References 29 publications

(31 reference statements)

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“…In the mentioned study, it has also been shown that the serum NO concentration is not different between SMexposed individuals and controls, regardless of skin disorders [12]. In the present study, a significant association was seen between the elevation of serum levels of NO and the occurrence of skin disorders in the SM-exposed group.…”

Section: P1: Comparison Of the Serum Level Of No Between Participantssupporting

confidence: 69%

“…A total of 100μL of the sample was mixed with 100 μL of Griess reagent (1% sulfanilamide in 5% phosphoric acid and 0.1% naphthyl enediamide dihydrochloride in water) and incubated at room temperature for 10 min followed by measuring the absorbance in a plate reader at 540nm (Stat-Fax 2100). Nitrite concentration in the samples was determined using a standard curve generated by different concentrations of sodium nitrite [12].…”

Section: Nitrite Assaymentioning

confidence: 99%

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Association of Nitric Oxide With Delayed Skin Problems After Sulfur Mustard Exposure: Part of Sardasht-Iran Cohort Study

et al. 2019

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Background: Exposure to Sulfur Mustard (SM) leads to short-and long-term adverse effects on various organs, including the skin. Despite several studies on long-term clinical manifestations of skin toxicity in SM-exposed individuals, the pathogenesis of SM-induced skin disorders is not fully understood. Materials and Methods:As part of Sardasht-Iran Cohort Study (SICS), this study aimed to find out the possibility of any correlation between the serums level of Nitric Oxide (NO) and skin problems due to the long-term effect of SM as well as the kind of skin illness. In this historical cohort study, 372 male SM-exposed subjects and 128 age-matched unexposed controls were studied. Clinical evaluation was carried out for all participants, and their serum concentration of NO was measured.Results: According to our results, the Mean±SD serum level of NO in the exposed group with skin disorders were significantly higher than that in the exposed group without skin disorders (1483.00±488.754µg/mL vs. 1364.50±487.887µg/mL; P=0.024). Also, among the exposed group, there was a significant elevation of serum NO associated with the type of lesion. For ezxample, specific lesions like mustard scar were associated with higher levels of NO compared to non-specific lesions like xerosis, itching, seborrheic dermatitis, etc. Also, a significant elevation in serum NO levels was found in the exposed subjects with pigmentation disorders (both hypo-and hyper-pigmentation) compared to the exposed participants without these skin problems (P<0.05). Finally, a significant difference in the serum level of NO was seen between the SM-exposed and the control subjects with no cherry angioma (P<0.05). Conclusion:Our results show the highest serum level of NO in the exposed group with specific lesions and the lowest or normal level of NO in the unexposed group with no skin illness. The elevated serum levels of NO may be associated with the progression of some skin complications in the SM-exposed subjects. This finding serves as a basis for further research on the molecular mechanisms and pathways involved in the pathogenesis of skin disorders in SM-exposed patients.

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Section: P1: Comparison Of the Serum Level Of No Between Participantssupporting

confidence: 69%

Section: Nitrite Assaymentioning

confidence: 99%

Association of Nitric Oxide With Delayed Skin Problems After Sulfur Mustard Exposure: Part of Sardasht-Iran Cohort Study

et al. 2019

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“…C-reactive protein, a non-specific marker of systemic inflammation, is also increased in patients with COPD due to SM poisoning, at levels comparable to the severity of disease [13]. Similarly, serum levels of the pro-apoptotic protein, soluble Fas ligand, are elevated in long-term survivors of SM exposure with persistent abnormalities in pulmonary function [14]. Pulmonary fibrosis following SM exposure is also correlated with increases in inflammatory cytokines and chemokines in bronchoalveolar lavage fluid (BAL), including IL-1α, IL-1β, IL-5, IL-6, IL-8, IL-12, IL-13, tumor necrosis factor (TNF)-α, CCL5, and CCL11 [15, 16].…”

Section: Acute and Chronic Pulmonary Effects Of Sm In Humansmentioning

confidence: 99%

Sulfur mustard-induced pulmonary injury: Therapeutic approaches to mitigating toxicity

Weinberger¹,

Laskin²,

Sunil³

et al. 2011

Pulmonary Pharmacology & Therapeutics

101

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Sulfur mustard (SM) is highly toxic to the lung inducing both acute and chronic effects including upper and lower obstructive disease, airway inflammation, and acute respiratory distress syndrome, and with time, tracheobronchial stenosis, bronchitis, and bronchiolitis obliterans. Thus it is essential to identify effective strategies to mitigate the toxicity of SM and related vesicants. Studies in animals and in cell culture models have identified key mechanistic pathways mediating their toxicity, which may be relevant targets for the development of countermeasures. For example, following SM poisoning, DNA damage, apoptosis, and autophagy are observed in the lung, along with increased expression of activated caspases and DNA repair enzymes, biochemical markers of these activities. This is associated with inflammatory cell accumulation in the respiratory tract and increased expression of tumor necrosis factor-α and other pro-inflammatory cytokines, as well as reactive oxygen and nitrogen species. Matrix metalloproteinases are also upregulated in the lung after SM exposure, which are thought to contribute to the detachment of epithelial cells from basement membranes and disruption of the pulmonary epithelial barrier. Findings that production of inflammatory mediators correlates directly with altered lung function suggests that they play a key role in toxicity. In this regard, specific therapeutic interventions currently under investigation include anti-inflammatory agents (e.g., steroids), antioxidants (e.g., tocopherols, melatonin, N-acetylcysteine, nitric oxide synthase inhibitors), protease inhibitors (e.g., doxycycline, aprotinin, ilomastat), surfactant replacement, and bronchodilators. Effective treatments may depend on the extent of lung injury and require a multi-faceted pharmacological approach.

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“…Ray et al [31], also reported that acute exposure to various mustard concentrations would induces apoptotic pathway in normal human bronchial epithelial cells and small airway epithelial cells via caspase-mediated pathway in vitro. A recent study reported that soluble FasL was increased in serum of SM-exposed patients [32]. …”

Section: Discussionmentioning

confidence: 99%

“…The main findings of lavage fluid of sulfur mustard-injured patients are inflammation, tissue damage, and neutrophil excess [46]. The neutrophils were shown to produce several cytokines such as tumor necrosis factor and transforming growth factor- β , as an inflammatory factor [50], and express Fas ligand [32, 50]. A study shows that transforming growth factor- β plays a pivotal role in bronchiolitis obliterans pathogenesis [51].…”

Section: Discussionmentioning

confidence: 99%

The Role of Fas-FasL Signaling Pathway in Induction of Apoptosis in Patients with Sulfur Mustard-Induced Chronic Bronchiolitis

Pirzad

Jafari

Tavana

et al. 2010

Journal of Toxicology

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Sulfur mustard (SM) is an alkylating agent that induces apoptosis and necrosis in cells. Fas-Fas ligand (FasL) interaction could induce apoptosis as well. In this study, it was hypothesized that apoptosis might play an important role in the pathogenesis of SM-induced lung injury via Fas-FasL signaling pathway. In a case-control study, Fas and FasL levels, caspase-3 activity and percent of apoptotic cells were measured in bronchoalveolar lavage (BAL) fluid of patients 20 years after exposure to sulfur mustard and compared with the control group. Results show that Fas and FasL levels were significantly higher in BAL fluid cells in patients group compared with the control (P = .001). No significant differences were observed between mild and moderate-severe groups. BAL fluid cells caspase-3 activity was not significantly different among the mild, moderate-severe, and control groups. The data suggest that Fas-FasL-induced apoptosis was impaired in BAL fluid cells of SM-exposed patients which might be one of the initiators of pathogenesis in SM-induced lung injury in these patients.

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Serum soluble Fas ligand and nitric oxide in long-term pulmonary complications induced by sulfur mustard: Sardasht-Iran Cohort Study

Cited by 20 publications

References 29 publications

Association of Nitric Oxide With Delayed Skin Problems After Sulfur Mustard Exposure: Part of Sardasht-Iran Cohort Study

Association of Nitric Oxide With Delayed Skin Problems After Sulfur Mustard Exposure: Part of Sardasht-Iran Cohort Study

Sulfur mustard-induced pulmonary injury: Therapeutic approaches to mitigating toxicity

The Role of Fas-FasL Signaling Pathway in Induction of Apoptosis in Patients with Sulfur Mustard-Induced Chronic Bronchiolitis

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