Sulphur Mustard Induced Toxicity, Mechanism of Action and Current Medical Management

Pant, S. C.; Lomash, Vinay

doi:10.14429/dlsj.1.10089

Cited by 4 publications

(3 citation statements)

References 97 publications

(90 reference statements)

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“…Studie provedené na laboratorních potkanech udávají, že během 24 hodin je takto vyloučeno až 60 % absorbované dávky. Nejčastěji nacházenými metabolity jsou thiodiglykol sulfoxid, thiodiglykol a produkty enzymatického štěpení aduktů sirného yperitu a glutathionu enzymem cystathionin β-lyasou, EC 4.4.1.8 (5,20).…”

Section: Toxikokinetikaunclassified

Sulfur Mustard: Persisting Threat

Jost¹,

Múčková²,

Štětina³

et al. 2018

MMSL

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Section: Toxikokinetikaunclassified

Sulfur Mustard: Persisting Threat

Jost¹,

Múčková²,

Štětina³

et al. 2018

MMSL

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“…4 It is an alkylating agent that causes serious blisters upon contact with human skin. 5 SM has been used as Chemical Warfare (CW) agent. [6][7][8][9][10] During the First World War and the Iran-Iraq conflict, SM was used and still remains a threat to both civilians and military personnel.…”

Section: Introductionmentioning

confidence: 99%

Effectiveness of Cytoprotective Agents on Sulfur Mustard Induced Toxicity: The In vitro Model

Gupta

Kannan

Gupta

et al. 2019

Curr. Res. Pharm. Sci.

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Sulphur mustard (bis (2-chloroethyl) sulfide, SM) is a powerful vesicating chemical warfare agent that causes profound injuries to the eyes, lungs and skin. Despite intensive research following the first use of SM in World War I, there is still no useful pretreatment or therapeutic antidote available. This agent remains a constant chemical threat. A potential approach to combating the debiliting effects of this agent is the use of compounds that can react with this material before it interacts with critical macromolecules. Glutathione (GSH), a tripeptide that exists in high concentrations in cells, reacts with SM and is involved in SM detoxification. Amifostine is a synthetic aminothiol, has been extensively used as a radioprotector. This prompted us to evaluate the protective efficacy of GSH, Amifostine and DRDE-07 (S-2(2aminoethyl amino) ethyl phenyl sulfide) (synthesized in our lab) against SM toxicity in vitro in HeLa cell line. All these compounds are thiol group containing compounds. Pretreatment of HeLa cell with these cytoprotectants led to decrease in cytotoxicity after SM exposure. The protective efficacy of above compounds were evaluated against sulphur mustard using HeLa cells. The above compounds were added to the media 1 hr before the SM exposure and incubated for 24 hrs. cell viability by MTT assay and LDH leakage were measured as end point.

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“…Part of the toxicity of SM and HN2 may stem from depletion of cellular glutathione stores which, in turn, leads to the intracellular accumulation of reactive oxygen species (ROS) and oxidative DNA damage (Crater and Kannan, 2007; Pant and Lomash, 2016; Paromov et al, 2007). The combination of oxidative DNA damage and direct DNA alkylation leads to strand breaks and activates polymerases such as poly(adenosine diphosphate-ribose) polymerase (PARP).…”

Section: Introductionmentioning

confidence: 99%

Assessment of the time-dependent dermatotoxicity of mechlorethamine using the mouse ear vesicant model

Cuffari

Tumu

Pino

et al. 2018

Interdisciplinary Toxicology

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Mechlorethamine (HN2) is an alkylating agent and sulfur mustard gas mimetic which is also used in anticancer therapy. HN2 is associated with skin inflammation and blistering which can lead to secondary infections. The purpose of the present study was to investigate the time-dependent dermatotoxicity of HN2 using the mouse ear vesicant model (MEVM). To this end, our operational definition of dermatotoxicity included tissue responses to HN2 consistent with an increase in the wet weights of mouse ear punch biopsies, an increase in the morphometric thickness of H&E stained ear sections and histopathologic observations including tissue edema, inflammatory cell infiltration and vesication. The ears of male Swiss Webster mice were topically exposed to a single dose of HN2 (0.5 μmol/ear) or DMSO vehicle (5 μl/ear) or left untreated (naive). Mice were then euthanized at 15 min, 1, 2, 4, 8 or 24 hr following HN2 exposure. Compared to control ears, mouse ears exposed to HN2 at all time points showed an increase in wet weights, morphometric thickness, edema, inflammatory cell infiltration and signs of vesication. The incidence in tissue vesication sharply increased between 4 and 8 hr after exposure, revealing that tissue vesication is well established by 8 hr and remains elevated at 24 hr after exposure. It is noteworthy that, compared to control ears, mouse ears treated with DMSO vehicle alone also exhibited an increase in wet weights and morphometric thickness at 15 min, 1, 2 and 4 hr following treatment; however, these vehicle effects begin to subside after 4 hr. The results obtained here using the MEVM provide a more holistic understanding of the kinetics of vesication, and indicate that time points earlier than 24 hr may prove useful not only for investigating the complex mechanisms involved in vesication but also for assessing the effects of vesicant countermeasures.

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Sulphur Mustard Induced Toxicity, Mechanism of Action and Current Medical Management

Cited by 4 publications

References 97 publications

Sulfur Mustard: Persisting Threat

Sulfur Mustard: Persisting Threat

Effectiveness of Cytoprotective Agents on Sulfur Mustard Induced Toxicity: The In vitro Model

Assessment of the time-dependent dermatotoxicity of mechlorethamine using the mouse ear vesicant model

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