Date of Award
Master of Arts
Dr. David S. Reinhold
Dr. Susan R. Stapleton
Dr. Jay Means
Masters Thesis-Open Access
The purpose of this study was to investigate the possible mechanisms involved in the decrease in mutant frequency when cells are treated with two different types of carcinogens: chromium (VI) in combination with benzo(a)pyrene diol epoxide (BPDE). Three of our working hypotheses are: Cr alone or Cr and BPDE synergistically activate detoxifying enzyme glutathione-S-transferase (GST), Cr alone or Cr and BPDE act synergistically to inhibit cell cycle at the G1/S boundary thus allowing more time for DNA repair, and Cr alone or Cr and BPDE synergistically activate DNA repair systems which result in more efficient repair of DNA adducts.
The results from experiments measuring GST activity show that the activity of the enzyme is not influenced by the different treatments with carcinogens. The results for the experiments related to cell cycle arrest show that entry into S phase occurs at the same time for all conditions.
Codrea, "Mechanistic Studies on the Antagonistic Effect of Chromium on BPDE Mutant Frequency in Human Fibroblasts" (2002). Master's Theses. 4466.