114E-16 |
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B. VILLALÓN1, E. González-Jasso2, M. Ramos-Gómez1, L. M. Salgado3, F. G. Loarca-Piña4, and R. Reynoso1. (1) Research and Graduate Studies in Food Science, Universidad Autónoma de Querétaro, Centro Universitario, Querétaro, 76010, Mexico, (2) Research Center in Applied Science and Advanced, Instituto Politécnico Nacional, José Siurob 10, Col Alameda, Querétaro, 76040, Mexico, (3) Biochemistry Department, CINVESTAV, IPN, Av. IPN 2508, México City, 07000, Mexico, (4) Programa de Posgrado en Alimentos del Centro de la República, Universidad Autónoma de Querétaro. Facultad de Química, Centro Universitario, Cerro de las Campanas S/N, Querétaro, 76010, Mexico Epidemiologic studies have provided enough evidence that high intake of vegetables and fruits protect humans against certain types of cancer, including colon cancer. Among the various constituents of vegetables, lutein has been studied as an anticarcinogenic agent. However, little is known about the potential of lutein in inhibiting K-ras and B-catenin gene mutations during the process of carcinogenesis. The objective of the present study was to determine the effect of lutein intake on the frequency and type of genetic alterations found in dimethylhydrazine induced colon cancer. Colon tumors were induced by 8 doses of s.c. weekly injections of dimethylhydrazine (DMH, 21 mg/kg body weight) in male Sprague-Dawley rats. 0.002% lutein was administered in the basal diet for 8 weeks after the last DMH injection. The animals were sacrificed 4 weeks later and colons were immediately removed for gross tumor counting. DNA was isolated and screened by PCR-SSCP analysis. The results showed that lutein significantly decreased both the incidence and the mean tumor number when compared with the DMH group (P < 0.05). By PCR-SSCP analysis, the lutein-treated group showed different K-ras mutations when compared with the DMH-treated group, and were also different from the non-treated control animals. In a similar analysis for the B-catenin gene, lutein treatment decreased the genetic changes observed in the DMH-treated rats and the band pattern of the mutations was similar to the non-treated control group. Our results give further evidence of the potential chemoprotective effect of lutein on colon cancer. Moreover, the finding that there is a shift in the distribution of K-ras mutations in the group given DMH and post-treated with lutein has a potentially important implication regarding gene-diet interactions and the events that give rise to colon cancer.
Session 114E, Nutraceuticals & Functional Foods: Bioactivity measurement and mechanism
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