Background: Ulcerative colitis, characterized by chronic, relapsing, and remitting inflammation, is an established risk factor for colon cancer. High intake of dietary lutein has been consistently associated with a reduced risk for colon cancer in epidemiologic studies. However, it is unknown whether dietary lutein supplementation protects against colon carcinogenesis through the inhibition of colonic inflammation. Using an established dextran sulfate sodium (DSS)-induced colitis and associated colonic carcinoma mouse model, we evaluated the effects of dietary lutein supplementation at various doses on the DSS-induced inflammation, ulceration, hyperplasia, dysplasia, and cancers in the colon and rectum. Methods: One hundred fifty female 8-week old Swiss-Webster mice (FER-Taconic) were assigned to one of ten groups (n = 15 in each group) for 18 weeks as follows: 1) 0.002% of lutein in the diet plus DSS; 2) 0.01% of lutein plus DSS; 3) 0.02% of lutein plus DSS; 4) 0.1% of lutein plus DSS; 5) DSS only; 6) 0.002% of lutein; 7) 0.01% of lutein; 8) 0.02% of lutein; 9) 0.1% of lutein; and 10) control without treatment. At week 4, the mice in groups 1-5 were provided with DSS for 4 cycles (1 cycle = 1 week 3% of DSS in drinking water followed by 2-week water) to initiate colitis and colorectal carcinoma. Results: Dietary lutein supplementation increased plasma and colonic lutein concentrations in mice in a dose-dependent fashion. Plasma and colonic lutein concentrations in the groups that were provided with both dietary lutein and DSS were slightly lower than the corresponding groups that were supplemented with dietary lutein only. All four doses of dietary lutein (0.002%, 0.01%, 0.02%, and 0.1%) were found to reduce significantly the DSS-induced hemocult, loose stool, and severe colorectal hyperplasia. Dietary lutein at all four doses also decreased the DSS-induced severe colorectal inflammation and dysplasia, but only the doses of 0.002% and 0.01% were significant. In addition, all four doses of dietary lutein nonsignficantly lowered the DSS-induced colorectal cancer. Dietary lutein had no effect on the DSS-induced colorectal ulceration, except for the 0.1% of lutein group, which had significantly reduced numbers of ulceration as compared with the DSS only group. There were no detectable colorectal ulceration, inflammation, hyperplasia, dysplasia, and cancers in the groups administrated with dietary lutein only and the control (groups 6-10). Conclusions: These data suggest that dietary lutein may provide a beneficial effect against the DSS-induced colorectal inflammation and associated cancer development in mice.
99th AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA