Protection Against the Acute and Delayed Toxicities of Sulfur Mustard
Abstract
Both the acute and delayed toxicities of DNA damaging agents like sulfur mustard (SM) appear to represent the outcome of a race between protective and toxic pathways triggered by DNA damage. Results obtained within the framework of our first objective to investigate the mechanisms involved in processing SM-induced DNA modifications, have revealed that both nucleotide excision repair (NER) and base excision repair (BER) are involved in processing SM-induced DNA damage. However, in contrast to the protective effect of NER, expression of the alkyl adenine DNA glycosylase, the first enzyme in the BER repair pathway, renders cells more sensitive to SM. We believe that specific post-exposure conditions can modulate cellular response to DNA damage by facilitating protective pathways and/or diminishing toxic ones. Specifically, as our second objective, we are exploring mild hypothermia as a means of ameliorating SM toxicity. Our results show that low temperature increases survival of mammalian cells after exposure to SM and suggest that, at least in part, this may be due to post-exposure modulation of DNA repair and replication.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2001
- Accession Number
- ADA391414
Entities
People
- Michael Volkert
- Zdenka Matijasevic
Organizations
- University of Massachusetts