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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 #156329
Title: SELENIUM (SE) AND SULFORAPHANE (SF) INTERACT TO REDUCE OXIDATIVE DAMAGE IN HT-29 CELLS

Author
item LEARY, PETE - UND, GRAND FORKS, ND
item HINTZE, KORRY - NDSU, FARGO, ND
item KECK, ANNA - UNIV OF ILLINOIS
item Wald, Karl
item Finley, John

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2003
Publication Date: 3/24/2004
Citation: Leary, P., Hintze, K.J., Keck, A., Wald, K., Finley, J.W. 2004. Selenium (se) and sulforaphane (sf) interact to reduce oxidative damage in ht-29 cells [abstract]. The Federation of American Societies for Experimental Biology Journal. 18:A916.

Interpretive Summary:

Technical Abstract: Selenium (Se) and the glucosinolate sulforaphane (Sf) interact to regulate the selenoprotein thioredoxin reductase (TR) in human hepatoma cells. Sf regulates transcription of TR mRNA as well as quinone reductase (QR) through an Antioxidant Response Element in the promoter region of both genes. Se modulates TR activity through a translational mechanism. To elucidate whether similar controls function in gut cells, Ht-29 colon carcinoma cells were cultured in media (n= 3-5 wells) containing: no added Se or Sf (control), 2.0 µM Se, 2.0 µM Sf or 2.0 µM Se + 2.0 µM Sf. Sf, but not Se, increased transcription of TR by 52% and QR by 61% (p<0.01) as assessed by luciferase reporter gene constructs. Activity of QR was increased 18% (p<0.05) by Sf. Activity of TR was increased 25% by Se, 28% by Sf, and 88% by Se + Sf (p<0.01). Oxidative DNA damage (COMET assay) was reduced 23% by the addition of Se, 36% with Sf, and 43% with Se and Sf (one-way ANOVA, p<0.05). These data suggest that Sf increases QR activity and Sf and Se interact to increase TR activity, resulting in increased protection of cultured gut cell DNA from oxidative damage.