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Antivesicant Strategies Based on DNA Repair and Apoptosis

Author: R RayK R BhatD S RosenthalB J BentonD R AndersonAll authors
Publisher: Ft. Belvoir Defense Technical Information Center 01 OCT 2005.
Edition/Format:   eBook : English
Database:WorldCat
Summary:
DNA is a major cellular target of the vesicant chemical warfare agent sulfur mustard (SM, bis-(2-chloroethyl) sulfide). Others and we have proposed a possible role of apoptosis in SM vesication. Our results suggest that in SM-exposed human epidermal keratinicytes (HEK), DNA damage, DNA repair, and apoptosis may be interdependent. In HEK, SM causes cell death accompanied by caspase-3 activation indicating apoptosis.  Read more...
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Material Type: Internet resource
Document Type: Internet Resource
All Authors / Contributors: R Ray; K R Bhat; D S Rosenthal; B J Benton; D R Anderson; W Holmes; J P Petrali; T Hamilton; P Ray; W J Smith; ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD.
OCLC Number: 227891134
Notes: See also ADM001851, Proceedings of the 2003 Joint Service Scientific Conference on Chemical & Biological Defense Research, 17-20 November 2003. The original document contains color images.
Description: 8 p.

Abstract:

DNA is a major cellular target of the vesicant chemical warfare agent sulfur mustard (SM, bis-(2-chloroethyl) sulfide). Others and we have proposed a possible role of apoptosis in SM vesication. Our results suggest that in SM-exposed human epidermal keratinicytes (HEK), DNA damage, DNA repair, and apoptosis may be interdependent. In HEK, SM causes cell death accompanied by caspase-3 activation indicating apoptosis. The general caspase inhibitor A-VAD-FMK (benzyl oxycarbonly-Val-Ala (o-methyl-fluromethylketone)) decreases not only SM induced apoptosis, but also protease stimulation consequent degradation of laminin-5 which maintains epidermal-dermal junction integrity. This knowledge may, therefore, be useful in developing successful antivesicant strategies.

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