skip to content
Protection Against the Vesicant Chemical Warfare Agent Sulfur Mustard: Therapeutics Utilizing Apoptosis Inhibitors. Preview this item
ClosePreview this item
Checking...

Protection Against the Vesicant Chemical Warfare Agent Sulfur Mustard: Therapeutics Utilizing Apoptosis Inhibitors.

Author: R RayB J BentonS L HauckC CarpinD S RosenthalAll authors
Publisher: Ft. Belvoir : Defense Technical Information Center, NOV 2006.
Edition/Format:   eBook : English
Database:WorldCat
Summary:
Sulfur mustard (SM, bis-(2-chloroethyl) sulfide), commonly called mustard gas, is a vesicant chemical warfare agent and a potential terrorism agent. SM is relatively easy to make and to deploy, which makes this chemical most likely to be used. SM exposure causes debilitating skin blisters (vesication) and injury to the eyes and the respiratory tract. Therefore, developing an effective medical countermeasure to  Read more...
Rating:

(not yet rated) 0 with reviews - Be the first.

Subjects
More like this

 

Find a copy online

Links to this item

Find a copy in the library

&AllPage.SpinnerRetrieving; Finding libraries that hold this item...

Details

Material Type: Internet resource
Document Type: Internet Resource
All Authors / Contributors: R Ray; B J Benton; S L Hauck; C Carpin; D S Rosenthal; ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD RESEARCH DIVISION.
OCLC Number: 318687425
Notes: Conference paper.
Description: 7 p. ; 23 x 29 cm.

Abstract:

Sulfur mustard (SM, bis-(2-chloroethyl) sulfide), commonly called mustard gas, is a vesicant chemical warfare agent and a potential terrorism agent. SM is relatively easy to make and to deploy, which makes this chemical most likely to be used. SM exposure causes debilitating skin blisters (vesication) and injury to the eyes and the respiratory tract. Therefore, developing an effective medical countermeasure to protect against the dermal, ocular and airway injuries due to this dreaded chemical agent is an urgent priority of the US Army. SM pathophysiology is consistent with epithelial cell damage, particularly basal cell apoptosis. SM-induced apoptosis may occur via multiple pathways dependent on one or more of the following: (a) abnormal Ca2+ homeostasis, (b) disturbed cellular bioenergetics, and (c) Fas (death receptor) response. Apoptosis pathways are characterized by the involvement of the pathway-specific caspases (cysteine aspartase). We determined caspase activity by assay of fluorogenic caspase type-specific peptide substrate hydrolysis. We studied caspase processing, i.e., proteolytic conversion of procaspase to active caspase by immunoblot analyses utilizing caspase type-specific antibodies. Our results in cell culture models of both human epidermal keratinocytes and human airway epithelial cells indicated that SM activates (a) caspase-9, an indicator of the Ca2+/CaM-mediated mitochondrial pathway, (b) caspase-8, a marker for the Fas-mediated pathway, and (c) caspase-3, the executioner caspase involved in both pathways. A peptide caspase inhibitor, specific for caspase-3 (ACDEVD-CHO), added to cells prior to SM decreased apoptosis. These observations suggest apoptosis as a mechanism of SM toxicity and caspase inhibitors as prospective medical countermeasures.

Reviews

User-contributed reviews
Retrieving GoodReads reviews...
Retrieving DOGObooks reviews...

Tags

Be the first.
Confirm this request

You may have already requested this item. Please select Ok if you would like to proceed with this request anyway.

Linked Data


<http://www.worldcat.org/oclc/318687425>
library:oclcnum"318687425"
library:placeOfPublication
library:placeOfPublication
owl:sameAs<info:oclcnum/318687425>
rdf:typeschema:Book
schema:about
schema:about
schema:about
schema:about
schema:about
schema:about
schema:about
schema:about
schema:about
schema:about
schema:bookFormatschema:EBook
schema:contributor
schema:contributor
schema:contributor
schema:contributor
schema:contributor
schema:contributor
schema:datePublished"2006"
schema:datePublished"NOV 2006"
schema:description"Sulfur mustard (SM, bis-(2-chloroethyl) sulfide), commonly called mustard gas, is a vesicant chemical warfare agent and a potential terrorism agent. SM is relatively easy to make and to deploy, which makes this chemical most likely to be used. SM exposure causes debilitating skin blisters (vesication) and injury to the eyes and the respiratory tract. Therefore, developing an effective medical countermeasure to protect against the dermal, ocular and airway injuries due to this dreaded chemical agent is an urgent priority of the US Army. SM pathophysiology is consistent with epithelial cell damage, particularly basal cell apoptosis. SM-induced apoptosis may occur via multiple pathways dependent on one or more of the following: (a) abnormal Ca2+ homeostasis, (b) disturbed cellular bioenergetics, and (c) Fas (death receptor) response. Apoptosis pathways are characterized by the involvement of the pathway-specific caspases (cysteine aspartase). We determined caspase activity by assay of fluorogenic caspase type-specific peptide substrate hydrolysis. We studied caspase processing, i.e., proteolytic conversion of procaspase to active caspase by immunoblot analyses utilizing caspase type-specific antibodies. Our results in cell culture models of both human epidermal keratinocytes and human airway epithelial cells indicated that SM activates (a) caspase-9, an indicator of the Ca2+/CaM-mediated mitochondrial pathway, (b) caspase-8, a marker for the Fas-mediated pathway, and (c) caspase-3, the executioner caspase involved in both pathways. A peptide caspase inhibitor, specific for caspase-3 (ACDEVD-CHO), added to cells prior to SM decreased apoptosis. These observations suggest apoptosis as a mechanism of SM toxicity and caspase inhibitors as prospective medical countermeasures."@en
schema:exampleOfWork<http://worldcat.org/entity/work/id/195775711>
schema:inLanguage"en"
schema:name"Protection Against the Vesicant Chemical Warfare Agent Sulfur Mustard: Therapeutics Utilizing Apoptosis Inhibitors."@en
schema:numberOfPages"7"
schema:publisher
schema:url
schema:url<http://handle.dtic.mil/100.2/ADA481694>

Content-negotiable representations

Close Window

Please sign in to WorldCat 

Don't have an account? You can easily create a free account.