Skip to main content
ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #141638
Title: EFFECT OF SELENIUM-ENRICHED BROCCOLI DIET ON DIFFERENTIAL GENE EXPRESSION IN MIN MOUSE LIVER

Author
item ZENG, HUAWEI
item Davis, Cindy
item Finley, John

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/2/2002
Publication Date: 3/14/2003
Citation: Zeng, H., Davis, C.D., Finley, J.W. 2003. Effect of selenium-enriched broccoli diet on differential gene expression in min mouse liver [abstract]. Journal of Federation of American Societies for Experimental Biology. 17(5):A1159.

Interpretive Summary:

Technical Abstract: Previous studies have shown that selenium (Se)-enriched broccoli can reduce colon cancer susceptibility in rodent models. It is not known whether this treatment also affects hepatic metabolism, which may be relevant in as much as colon cancer cells are known to metastasize to the liver. To better understand the protective role for selenium-enriched broccoli in tumorigenesis, a gene profile of the mouse liver was analyzed. Multiple intestinal neoplasia (Min) mice were fed diets with the same amounts of broccoli, with regular or high intrinsic selenium content, providing either 0.11 mg or 2.1 mg selenium/kg for 10 wk. Mouse pathway finder-1 GEArrays revealed that selenium-enriched broccoli moderately increased i(kappa)B(alpha),NF(kappa)B, hsp86 and gadd45 gene transcripts. In addition, an analysis of the binding of liver nuclear proteins to 32**P-labeled probes demonstrated that selenium-enriched broccoli enhanced the binding of transcription factor p53, NF(kappa)B and AP-1 to their cis-acting elements. Collectively, these results suggest for the first time that selenium-enriched broccoli can activate certain pro-apoptotic genes linked to p53, NF(kappa)B and stress signaling pathways in animals genetically susceptible to tumorigenesis.