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Effects of contaminated fish oil on aberrant crypt foci formation and colonic cell kinetics
Author(s) -
Kang Brian,
Kim Jinyoung,
Hoh Eunha,
Hong Mee Young
Publication year - 2012
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.26.1_supplement.1023.17
Subject(s) - azoxymethane , fish oil , aberrant crypt foci , corn oil , food science , crypt , polyunsaturated fatty acid , chemistry , biology , fish <actinopterygii> , colorectal cancer , cancer , carcinogenesis , biochemistry , fatty acid , endocrinology , fishery , colonic disease , genetics , gene
Fish oil is a rich source of n‐3 polyunsaturated fatty acids, which are known to prevent colon cancer. However this message is confounded by Food Drug Administration warnings which state that consumption of certain types of fish should be restricted due to contaminants such as polychlorinated biphenyls (PCBs). Therefore, this study examined the effects of fish oil contaminated with PCB (4000ng/ml fat) as compared to regular fish oil on the risk factors of colon cancer including aberrant crypt foci (ACF) formation and colonic cell kinetics (cell proliferation and apoptosis). Thirty Sprague‐Dawley rats were divided into three groups and fed corn oil, fish oil, or contaminated fish oil (PCB) for nine weeks and injected with saline or azoxymethane (2 times at wk 3 and 4). Fish oil‐fed rats had a lowered number of ACF (P=0.013) and high multiplicity ACF (P=0.024) compared to the corn oil and contaminated fish oil groups. Fish oil feeding resulted in lower cell proliferation index than corn oil and PCB groups (P=0.009). Cell apoptosis was not significantly different amongst any of the groups. These results suggest that dietary fish oil protects against colon cancer by lowering the number of early preneoplastic lesions through the inhibition of cell proliferation. PCB contaminated fish oil reduced the beneficial effects of fish oil on colon carcinogenesis. Supported by CHNR08‐810, SDSU UGP and NUTR 302L class.