CHED 593 |
| This work seeks to investigate the mechanism by which cyclophosphamide, a widely used chemotherapeutic agent, damages DNA. Like many anticancer drugs, cyclophosphamide results in the covalent linking of tumor DNA strands. This research investigated the extent to which other species present in cells affect the efficiency of this process. Glutathione, which is often present at high levels in tumor cells, is known to result in inactivation of cyclophosphamide. This study used a model system to investigate the competition between the beneficial DNA damaging reaction and the undesired deactivation of the drug by glutathione. The reactive species formed from cyclophosphamide in vivo was obtained by chemical synthesis. Imidazole and 2'-deoxyguanosine were used to model the nucleophilic sites found in the DNA double helix. At high glutathione concentrations, deactivation of the drug becomes significant; an observation which should guide the design of new treatments. |
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Undergraduate Research Poster Session: Organic Chemistry
11:00 AM-1:00 PM, Monday, March 26, 2007 Hyatt Regency Chicago -- Riverside Center, Poster
Division of Chemical Education |