Abstract
Colon cancer is the third leading cause of cancer related death in men and women in the United States. Data from multiple studies show that dietary fish oil is associated with a decrease in colon cancer incidence. Estradiol (E2) has also been demonstrated to be protective against colon tumor formation and we have shown that E2 induces colonocyte apoptosis in conjunction with reducing formation of premalignant lesions. To date, however, possible relationships between estrogen status and the benefits of fish oil have not been thoroughly examined. We hypothesized that E2 could enhance the effects of dietary fish oil by additively decreasing DNA damage and increasing apoptosis. Dietary fish oil significantly decreased immunohistochemical staining intensity of O6‐methyldeoxyguanosine DNA adducts independent of the presence of E2 at 9h and 12h post treatment with carcinogen. E2 resulted in a significant increase in apoptosis independent of diet group at 12h post carcinogen, most notably in the luminal third of the crypts. Fish oil was not associated with an increase in apoptosis. These data are important because they demonstrate that fish oil is protective against DNA damage in the colon regardless of E2 status. In addition, our data demonstrate that induction of apoptosis in colonocytes at the point of DNA damage may serve as a primary mechanism for how E2 suppresses colon tumor formation.Grant Funding Source: American Institute for Cancer Research
Published Version
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