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Dietary fish oil decreases DNA adducts in the rat colon independent of estrogen status
Author(s) -
Armstrong Cameron,
Allred Clinton D.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.727.4
Subject(s) - apoptosis , fish oil , dna damage , carcinogen , colorectal cancer , estrogen , cancer , programmed cell death , fish <actinopterygii> , medicine , biology , dna adduct , cancer research , endocrinology , physiology , chemistry , dna , biochemistry , fishery
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 (E 2 ) has also been demonstrated to be protective against colon tumor formation and we have shown that E 2 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 E 2 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 E 2 at 9h and 12h post treatment with carcinogen. E 2 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 E 2 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 E 2 suppresses colon tumor formation. Grant Funding Source : American Institute for Cancer Research