Background: Epidemiologic, clinical, and experimental studies have suggested that
fish oil (FO), a rich source of n-3 (ω-3)
polyunsaturated fatty acids, protects against
colon cancer. However, this message is confounded by the FDA's warning that the consumption of certain types of fish should be restricted because of contamination with
persistent organic pollutants (POPs), such as
polychlorinated biphenyls (
PCBs) and organochlorine pesticides.Objective: We examined FO contaminated with POPs (
PCBs, dichlorodiphenyltrichloroethane, and
chlordane) compared with unmodified FO on the risk factors of
colon cancer development.Methods: Male Sprague-Dawley rats aged 28 d (
n = 30) were allocated into 3 groups and fed 15%
corn oil (CO), FO, or POP-contaminated FO for 9 wk with a
subcutaneous injection of colon
carcinogen azoxymethane at weeks 3 and 4. Colonic
aberrant crypt foci (ACF) and cell proliferation were enumerated, and the gene expression of
inflammation,
antioxidant enzymes, and repair
enzymes were determined with the use of real-time quantitative polymerase chain reaction analysis.Results: FO-fed rats had a lower number of ACF (mean ± SE: 29 ± 4.0 for FO compared with 53 ± 8.4 for CO and 44 ± 4.6 for POP FO) and higher-multiplicity ACF than the CO and POP FO groups (4.7 ± 0.9 for FO compared with 11 ± 1.5 for CO and 9.6 ± 1.8 for POP FO) (P < 0.05). FO feeding lowered the proliferation index compared with the CO and POP FO feeding groups (18% ± 1.1% for FO compared with 25% ± 1.6% for CO and 23% ± 0.7% for POP FO) (P = 0.009).
Superoxide dismutase [2.4 ± 0.6 relative quantification (RQ) for FO compared with 1.2 ± 0.2 RQ for CO and 1.3 ± 0.3 RQ for POP FO] and
catalase gene expression (10 ± 2.0 RQ for FO compared with 5.4 ± 1.1 RQ for CO and 6.6 ± 1.5 RQ for POP FO) were higher in the FO group than in the CO and POP FO groups (P < 0.05). There were no differences between CO and POP FO on the variables.Conclusion: These results indicate that POPs in FO reduce the preventive effects of FO on colon
carcinogenesis by increasing preneoplastic lesion formation through the downregulation of
antioxidant enzyme expression and increasing cell proliferation in rats.