Antivesicant Strategies Based on Dna Repair and Apoptosis
نویسندگان
چکیده
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 keratinocytes (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 ZVAD-FMK (benzyl oxycarbonyl-Val-Ala-Asp (o-methyl-fluromethylketone)) decreases not only SM-induced apoptosis, but also protease stimulation and 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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