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THE ROLE OF CURCUMIN IN RESPONSE TO BPDE-INDUCED DNA DAMAGE IN HUMAN LUNG EPITHELIAL CELLS Erica Nicole Rogers July 20, 2011 Long-term exposure to harmful carcinogens like benzo[a]pyrene (BaP) are linked to lung cancer. Benzo[a]pyrene diol epoxide (BPDE), the ultimate carcinogen produced by BaP bioactivation, is believed to play an important role in lung carcinogenesis. The tumor suppressor protein is p53 signals cell cycle arrest, DNA repair, and apoptosis in response to BPDE-induced damage. However, physiological exposure to BPDE fails to activate p53. Although the bioactive principle of turmeric spice, curcumin, shows promising effects against BPDE-induced carcinogenesis, its exact mode of action remains unclear. Therefore the aim of this dissertation was to investigate whether curcumin prevents BPDE-induced DNA damage by regulating p53-mediated cellular responses in A549/LXSN (p53+) and A549/E6 (p53-) cells. I hypothesize that curcumin may reduce BPDE-induced DNA damage by lowering the threshold of p53 activation, thereby inducing p53-mediated mechanisms. Curcumin pretreatment reduced BPDEDNA adducts in a p53-dependent manner. However, p53-regulated proteins XPC and DDB2 did not change with curcumin pretreatment and p53-expression. Curcumin pretreatment did not change the overall repair rate in p53+ cells. Curcumin pretreatment, p53-expression, and BPDE exposure did not significantly change glutathione-S-

The role of curcumin in response to BPDE-induced DNA damage in human lung epithelial cells.