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DNA Damage-Induced Apoptosis: Inhibition by Calmodulin Antagonist, Fas Receptor Antibody and Caspase Inhibitors.

Author: R RayB J BentonM E BurkeT RockwoodK R BhatAll authors
Publisher: Ft. Belvoir : Defense Technical Information Center, 01 JUL 2003.
Edition/Format:   eBook : English
Database:WorldCat
Summary:
Sulfur mustard (HD, bis-(2-chloroethyl) sulfide) is a vesicant that causes DNA strand breaks and apoptosis in cultured normal human epidermal keratinocytes (NHEK). HD causes apoptosis via two independent pathways, a Ca2+/calmodulin (CaM)-mediated mitochondrial pathway and Fas receptor (CD95) pathway. We studied the effects of the exogenously added CaM antagonist W7, the CD95 antibody, the caspase-3 inhibitor  Read more...
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Material Type: Internet resource
Document Type: Internet Resource
All Authors / Contributors: R Ray; B J Benton; M E Burke; T Rockwood; K R Bhat; D R Anderson; J P Petrali; W J Smith; P Ray; D S Rosenthal; ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD.
OCLC Number: 318689915
Notes: Conference paper.
Description: 7 pages ; 23 x 29 cm

Abstract:

Sulfur mustard (HD, bis-(2-chloroethyl) sulfide) is a vesicant that causes DNA strand breaks and apoptosis in cultured normal human epidermal keratinocytes (NHEK). HD causes apoptosis via two independent pathways, a Ca2+/calmodulin (CaM)-mediated mitochondrial pathway and Fas receptor (CD95) pathway. We studied the effects of the exogenously added CaM antagonist W7, the CD95 antibody, the caspase-3 inhibitor Ac-DEVD-CHO, and the general caspase inhibitor Z-VAD-fmk on NHEK viability loss (Calcein AM fluorescence assay, LDH release assay) due to HD. All protected against HD. Z-VAD-fmk was the most effective. These results provide a logical approach toward developing an anti-apoptotic vesicant countermeasure.

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Primary Entity

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