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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 #116840


item Uthus, Eric
item Davis, Cindy
item Yokoi, Katsuhiko

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/10/2000
Publication Date: 3/7/2001
Citation: Uthus, E.O., Davis, C.D., Yokoi, K. 2001. Selenium deprivation decreases the activity of liver betaine homocysteine methyltransferasein rats [abstract]. The Federation of American Societies for Experimental Biology Journal. 15:A969.

Interpretive Summary:

Technical Abstract: Selenium (Se) deprivation causes a marked reduction in plasma homocysteine (Hcys). To understand the causes and consequences of decreased Hcys concurrent with Se deficiency, betaine homocysteine methyltransferase (BHMT (one of the enzymes that synthesizes methionine from homocysteine) was measured. The experiment used groups of male weanling Fisher-344 rats (N=7- -8/group) fed a basal torula yeast, Se-deficient diet supplemented with 0, 0.02, 0.05, or 0.1 mg Se (as sodium selenite)/kg diet. The basal diet contained 1.5+/-0.3 ng Se/g; rats were fed for 62 days. Plasma Hcys concentration and the activities of glutathione peroxidase (GPx) and BHMT decreased with decreasing dietary selenium with values from the 0 Se group being markedly lower, especially compared to values from the rats fed 0.05 0.1 Se. In contrast, the concentration of plasma total free glutathione (GS increased significantly in the 0 Se animals. The mechanism leading to a decrease in plasma Hcys as a result of Se deficiency is unknown. Possibly, less Hcys is remethylated to form methionine (as suggested by a decreased specific activity of BHMT), and more is being routed through the transsulfuration pathway (as indicated by the increase in GSH).