Antivesicant Strategies Based on DNA Repair and Apoptosis
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.
"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."@en
ARMY MEDICAL RESEARCH INST OF CHEMICAL DEFENSE ABERDEEN PROVING GROUND MD.
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