Increase in oxidative stress via glutathione modulation as a novel approach to enhance cancer sensitivity to doxorubicin

MEDI 344

Teresa Seefeldt, Teresa.Seefeldt@sdstate.edu, Yong Zhao, Wei Chen, Laura Carlson, Adam Stoebner, Sarah Hanson, Ryan Foll, Srinath Palakurthi, and Xiangming Guan. Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Box 2202 C, Brookings, SD 57007
Drug resistance is a major cause of cancer treatment failure. Doxorubicin induces the production of damaging reactive oxygen species as part of its mechanism of action, and resistance to doxorubicin can develop through increased levels of the intracellular antioxidant glutathione. Mechanisms of increasing the state of oxidative stress could enhance the sensitivity of cancer cells toward doxorubicin. Modulation of intracellular glutathione via a combination of glutathione reductase inhibition and glutathione synthesis inhibition is a novel approach to increasing oxidative stress and improving the activity of cancer chemotherapy. A novel irreversible glutathione reductase inhibitor, 2-acetylamino-3-[4-(2-acetylamino-2-carboxyethylsulfanylthiocarbonylamino)phenylthiocarbamoylsulfanyl]propionic acid (2-AAPA), and a glutathione synthesis inhibitor, buthionine sulfoximine (BSO) were used to increase the oxidative state in OVCAR-3 cells followed by treatment with doxorubicin. The combination exhibited a higher synergistic effect with doxorubicin than either compound alone. The methods and results will be presented.
 

Poster Session
7:00 PM-9:00 PM, Wednesday, August 22, 2007 BCEC -- Exhibit Hall - B2, Poster

Division of Medicinal Chemistry

The 234th ACS National Meeting, Boston, MA, August 19-23, 2007